Acute coronary syndrome: current standards for diagnosis and treatment. Treatment of acute coronary syndrome (prehospital stage) Clinical variants of myocardial infarction
Acute coronary syndrome (ACS) - group clinical signs or symptoms suggestive of myocardial infarction (MI) or unstable angina (UA).
Classification
Acute coronary syndromes:
1. OKS with ST segment elevation
A) MI with ST segment elevation
Q-wave MI
MI without Q wave
B) Prinzmetal's angina
B) Pericarditis
D) Early repolarization syndrome
2.)ACS without ST segment elevation
MI without Q wave
Unstable angina
Treatment tactics depending on the type of ACS
The results of ACS treatment largely depend on the correct actions of the doctor at the prehospital stage.
The main task of the ambulance doctor is effective relief pain syndrome and, perhaps
early reperfusion therapy.
Algorithm for the treatment of patients with ACS
Sublingual nitroglycerin (0.4 mg) or nitroglycerin spray every five minutes. After taking three doses with persistent pain in the chest and systolic blood pressure less than 90 mm Hg. Art. it is necessary to resolve the issue of prescribing nitroglycerin intravenously as an infusion.
The drug of choice for the relief of pain is morphine sulfate, 10 mg intravenously in a stream in physiological sodium chloride solution.
Early appointment of acetylsalicylic acid at a dose of 160-325 mg (chew). Patients who have previously taken aspirin can be given clopidogrel 300 mg followed by a dose of 75 mg/day.
The immediate appointment of β-blockers is recommended for all patients, if there are no contraindications to their use (atrioventricular blockade, bronchial asthma history of acute left ventricular failure). Treatment should begin with short-acting drugs: propranolol at a dose of 20-40 mg or metroprolol (egilok) 25-50 mg orally or sublingually.
Elimination of factors that increase the load on the myocardium and contribute to increased ischemia: hypertension, heart rhythm disturbances.
Further tactics of helping patients with ACS, as already mentioned, is determined by the characteristics of the ECG picture.
Patients with clinical signs of ACS with persistent ST-segment elevation or acute left bundle branch block, in the absence of contraindications, need to restore the patency of the coronary artery using thrombolytic therapy or primary percutaneous angioplasty.
When possible, thrombolytic therapy (TLT) is recommended at the prehospital stage. If TLT can be performed within the first 2 hours after the onset of symptoms (especially within the first hour), it can stop the development of MI and significantly reduce mortality. TLT is not performed if more than 12 hours have passed since the anginal attack, except when ischemic attacks continue (pain, ST segment elevations).
20. Unstable angina (NSK)) - most difficult period exacerbations coronary disease
heart disease (CHD), leading to the development of myocardial infarction (MI) or sudden death. NSC - by
clinical manifestations and prognostic value is intermediate between
the main clinical and morphological forms of coronary artery disease - stable angina pectoris and acute myocardial infarction
myocardium.
Classification of unstable angina (Hamm C. W., Braunwald E.)
All patients with NSC are subject to urgent hospitalization in wards (blocks) of intensive observation and treatment. In parallel with the treatment, an ECG recording is performed in dynamics, a complete blood count, determination of the activity of cardiospecific enzymes, if possible, echocardiography, myocardial scintigraphy. Round-the-clock clinical and monitoring supervision.
The goals of treatment are to relieve pain, prevent recurrent angina attacks, and prevent the development of acute MI and related complications. Treatment should begin with aspirin. The antithrombotic effect of ASA is based on the irreversible inhibition of platelet cyclooxygenase. As a result, platelets lose their ability to synthesize thromboxane A2 (TXA2), which induces platelet aggregation and has vasoconstrictive properties. As a result, the possibility of platelet aggregation and thrombus formation is reduced.
In the presence of coronary pain at the time of admission, the patient is given nitroglycerin 0.5 mg under the tongue, after 10-15 minutes. it can be repeated. With insufficient effect, neuroleptanalgesia is performed, as with MI. At the same time, intravenous infusions of nitroglycerin and heparin are prescribed. The initial dose of nitroglycerin preparations (1% solution of nitroglycerin, perlinganite, or isosorbite dinitrate-isoket) is 5-15 mcg / min, then every 5-10 minutes. the dose is increased by 10-15 mcg / min., not allowing a decrease in systolic blood pressure less than 100-90 mm. rt. Art.
Beta-blockers are important in the treatment of NSCs. They contribute to the elimination of myocardial ischemia, prevent sudden hemodynamic changes, reduce vascular damage, inhibit the formation of lipid plaques, are prophylactic agents in relation to the deepening, expansion or repetition of an existing rupture and to ruptures of other plaques, and have an antiarrhythmic effect.
The initial use of beta-blockers in combination with aspirin, heparin can be used in cases where patients with NSC have hyperactivity of the sympathetic nervous system, manifested by tachycardia, hypertension, rhythm disturbance. In these cases, oral beta-blockers may be used, and intravenous administration may also be recommended.
In spontaneous angina pectoris, Prinzmetal-type angina pectoris, calcium antagonists are used, of which the dihydropyridine group - nifedipine is indicated only for this variant of NSC. In order to stop an attack of coronary pain, nitroglycerin is given, with insufficient effectiveness - nifedipine, offering the patient a tablet to chew for better absorption in the oral cavity. For the prevention of seizures, nitrates or calcium antagonists are prescribed, preferably prolonged ones (amlodipine, lomir, etc.); verapamil, dilgiazem can be used. Beta-blockers with "pure" vasospastic form of NSC can worsen coronary blood flow. Beta-blockers are considered contraindicated in those patients with spontaneous angina pectoris in whom spasm of the large coronary arteries is documented on coronary angiography using an ergometrine test.
In cases where there is no evidence of NSC progression at the time of hospitalization, especially when the last angina attack was 48 hours later, there are no ECG changes, there is no increase in cardio-specific enzymes, treatment may be limited to aspirin in combination with beta-blockers, and / or nitrates. In some cases, calcium antagonists can be used - veripamil, diltiazem, but not nifedipine. Especially in cases where beta-blockers are contraindicated. These calcium antagonists can be combined with nitrates.
In violation of the heart rhythm, antiarrhythmic treatment is carried out, including electro-pulse therapy.
In cases where within 48-72 hours, despite active therapy, angina attacks do not change the intensity and duration, there are indications for performing urgent coronary angiography and discussing the issue of surgical treatment.
An alternative to surgical treatment of NJC is currently PTCA and intracoronary prosthesis using intravascular prostheses (stents). Indications for its implementation are proximal single-vessel stenoses of at least 50% of the lumen of the vessel
Thus, the sequence of therapeutic measures in the treatment of NSC can be represented as follows: hospitalization in the ICU, the appointment of aspirin, nitroglycerin, heparin, beta-blockers; with vasospastic variants of NSC - nitroglycerin, calcium antagonists; in acute coronary syndrome with ST segment elevation or fresh blockade of the left bundle branch block - the use of thrombolytic drugs. In the future, the use of blockers of platelet glycoprotein receptors II beta / III alpha and low molecular weight heparins. With the ineffectiveness of drug therapy - surgery(CABG, PTCA, intracoronary prosthetics - stents). Further, the transition to planned treatment according to the generally accepted method for chronic coronary artery disease.
21. Myocardial infarction (MI) - This is an acute focal necrotic lesion of the heart muscle.
Risk factors
Tobacco smoking and passive smoking, arterial hypertension, increased concentration
LDL cholesterol ("bad" cholesterol) in the blood, low concentration of HDL cholesterol
("good" cholesterol) in the blood, high blood triglycerides, low physical
activity, age, air pollution, men are more likely to suffer from myocardial infarction than
women, obesity, alcoholism, diabetes mellitus, myocardial infarction in the past and manifestation
any other manifestations of atherosclerosis
CLASSIFICATION
By stages of development:
Prodromal period (0-18 days)
Acute period (up to 2 hours from the onset of MI)
Acute period (up to 10 days from the onset of MI)
Subacute period (from 10 days to 4-8 weeks)
Scarring period (from 4-8 weeks to 6 months)
According to the anatomy of the lesion:
transmural
intramural
Subendocardial
Subepicardial
In terms of damage:
Large-focal (transmural), Q-infarction
Small-focal, non-Q-infarction
Localization of the focus of necrosis.
Myocardial infarction of the left ventricle (anterior, lateral, inferior, posterior).
Isolated apical myocardial infarction.
Myocardial infarction of the interventricular septum (septal).
Myocardial infarction of the right ventricle.
Combined localizations: posterior-inferior, anterior-lateral, etc.
With the flow:
Monocyclic
lingering
Recurrent MI (in 1 y coronary artery sprinkles, a new focus of necrosis from 72 hours to 8 days)
Repeated MI (in other short art., a new focus of necrosis 28 days after the previous MI)
Clinical classification prepared by the joint working group European Society cardiologists, American College of Cardiology, American Heart Association and World Heart Federation (2007):
Spontaneous MI (type 1) associated with ischemia due to a primary coronary event such as plaque erosion and/or rupture, cracking or dissection.
Secondary MI (type 2) associated with ischemia caused by an increase in the lack of oxygen or its supply,
Sudden coronary death (type 3), including cardiac arrest,
PCI-associated MI (type 4a).
MI associated with stent thrombosis (type 4b), which is confirmed by angiography or autopsy.
CABG-associated MI (type 5).
Pathogenesis
There are stages:
1) Ischemia 2) Damage (necrobiosis) 3) Necrosis 4) Scarring
Ischemia can be a predictor of a heart attack and last quite a long time. At the heart of the process is a violation of myocardial hemodynamics. The narrowing of the lumen of the artery of the heart to such an extent that the restriction of blood supply to the myocardium can no longer be compensated is usually considered clinically significant. Most often this occurs when the artery is narrowed by 70% of its cross-sectional area. When compensatory mechanisms are exhausted, they speak of damage, then metabolism and myocardial function suffer. Changes can be reversible (ischemia). The stage of damage lasts from 4 to 7 hours. Necrosis is characterized by irreversible damage. 1-2 weeks after the infarction, the necrotic area begins to be replaced by scar tissue. The final formation of the scar occurs after 1-2 months.
22. Clinical picture of acute MI. The most typical manifestation of myocardial infarction is chest pain. The pain “radiates” along the inner surface of the left hand, producing tingling sensations in the left hand, wrist, fingers. Other possible areas of irradiation are the pleural girdle, neck, jaw, interscapular space, also predominantly on the left. Thus, both localization and irradiation of pain does not differ from an angina attack.
Pain in myocardial infarction is very strong, perceived as a dagger, tearing, burning, "a stake in the chest." Sometimes this feeling is so unbearable that it makes you scream. As with angina pectoris, it may not be pain, but discomfort in the chest: a feeling of strong compression, pressure, a feeling of heaviness "pulled with a hoop, squeezed in a vise, crushed with a heavy plate." Some people experience only a dull ache, numbness in the wrists, combined with severe and prolonged chest pain or discomfort in the chest.
The onset of anginal pain in myocardial infarction is sudden, often at night or early morning. Pain sensations develop in waves, periodically decrease, but do not stop completely. With each new wave, pain or discomfort in the chest intensifies, quickly reaches a maximum, and then weakens.
Pain or discomfort in the chest lasts more than 30 minutes, sometimes for hours. It is important to remember that for the formation of a myocardial infarction, the duration of anginal pain for more than 15 minutes is sufficient. Another important hallmark of myocardial infarction is the lack of reduction or cessation of pain at rest or when taking nitroglycerin (even repeatedly).
Clinical variants of myocardial infarction:
asthmatic variant characterized by the development of an attack of cardiac asthma or pulmonary edema (see the relevant section). More common in older patients;
gastralgic(abdominal) variant begins with pain in the epigastrium and behind the sternum, nausea, and maybe vomiting. Sometimes the pain radiates to the lower abdomen, signs of dynamic intestinal obstruction may appear. It is especially difficult to recognize this variant of myocardial infarction in patients with gastric ulcer and duodenum in history. However, palpation of the abdomen in this case does not cause significant pain, the abdomen is soft, there are no symptoms of peritoneal irritation, which does not correspond to the patient's complaints of very severe pain. (Just do not forget that myocardial infarction and acute surgical diseases can occur at the same time!);
cerebral variant manifests itself as an acute violation of cerebral circulation. There may be loss of consciousness, epileptiform convulsions, impaired speech, paresis and paralysis. This can be explained both by the simultaneous development of myocardial infarction and stroke (vasospasm or the ingress of blood clots simultaneously into the vessels of the heart and brain), and by complications of MI, for example, Morgagni-Adams-Stokes syndrome (arrhythmia), which caused cerebral hypoxia;
arrhythmic variant - the appearance for the first time of various disturbances of rhythm and conduction;
painless(atypical) variant of myocardial infarction is manifested only by changes in the ECG, sometimes detected by chance.
23. ECG : In the sharpest stages (damage stages, most often from 20 minutes to 2 hours) - in ECG leads recorded above the infarct area - a monophasic curve: the ST segment is sharply raised above the isoline, forms an arc, convex upward, merging directly with a high positive T wave. In acute stage of MI, which lasts up to 10 days (usually one week), a focus of necrosis is formed. At the same time, the ECG records pathological deep and wide Q wave and R wave decreases. The deeper and wider the Q wave, the smaller the R wave, and in transmural infarction, the R wave R at all disappears. The ST segment begins to gradually decline, but remains above the isoline, and the tooth T becomes negative. In leads opposite to the localization of MI, on the ECG are recorded reciprocal changes. In the acute period of MI, they are the reverse of the main ones. In subacute stage in the leads recorded above the MI area, the QRS complex remains the same, as in the acute stage, the ST segment is close to the isoelectric line, the T wave is deep, negative, equilateral ("coronary" Purdy's wave). The duration of this stage is 4-5 weeks.
In the stage of scarring, the QRS complex remains the same as in subacute stage, but after a year or more, the pathological Q wave may decrease or even disappear, and the R wave voltage may increase slightly. This is explained by compensatory myocardial hypertrophy in the area of the scar. The ST segment is on the isoelectric line, T becomes less negative, or smoothed, or even slightly positive. The duration of this stage is on average 8 weeks or more from the onset of myocardial infarction. The main sign of the cicatricial stage is the absence of further ECG dynamics.
Laboratory data
Within a few hours after the development of MI, the number of leukocytes in the blood increases and persists for 3-7 days mainly due to neutrophils (leukocyte formula shift to the left). The first days of the disease are characterized by a decrease in the number of eosinophils up to aneosinophilia. ESR in the first days remains normal and begins to increase after 1-2 days, after an increase in temperature and an increase in the number of leukocytes. By the end of the week, leukocytosis decreases and ESR increases ("scissors symptom"). The maximum ESR is usually observed between the 8th and 12th day of illness, then gradually decreases and returns to normal after 3-4 weeks.
The most valuable method laboratory diagnostics THEM– study of the activity of blood serum enzymes. Early and informative in terms of diagnostics is the determination of troponin-T. It appears after 6-8 hours, reaches a maximum after 24-36 hours and remains elevated for 10-14 days.
Increases the activity of creatine phosphokinase (CPK), especially its isoenzyme - MB. It is noted already after 6-8 hours from the onset of MI and normalizes for 2-3 days. Aminotransferases are increased (especially AST and, to a lesser extent, ALT). In AST, the initial increase is noted after 8-12 hours, the maximum rise is on the 2nd day and normalizes by the 3-7th day. The activity of lactate dehydrogenase (especially the first isoenzyme - LDH 1) increases after 24-48 hours from the onset of the disease, the maximum increase by 3-5 days and normalizes by 8-15 days. The content of sialic acids and C-reactive protein in the blood serum also increases, which are kept at elevated numbers for up to 2 weeks.
Widely used to diagnose MI definition myoglobin in the blood, which normally does not exceed 85 ng / ml. An important advantage of this test is its early appearance: on average, 2-3 hours earlier than the increase in the activity of the "earliest" of the enzymes - CPK-MB.
From others additional methods diagnostics, radioisotope research methods have the highest "resolving" ability, in particular, scintigraphy with technetium and waist . It allows diagnosing MI where other methods are powerless.
Treatment for MI
1. Relief of pain syndrome.
2. Restoration of coronary blood flow.
3. Reducing the work of the heart and myocardial oxygen demand.
4. Limiting the size of myocardial infarction.
5. Treatment and prevention of complications of myocardial infarction.
1.Morphine intravenously fractionally
Adequate pain relief, reduction of pre- and afterload, psychomotor agitation, myocardial oxygen demand (2-5 mg intravenously every 5-15 minutes until the pain syndrome is completely eliminated or until side effects appear)
2.C treptokinase (streptase)
Restoration of coronary blood flow (thrombolysis), relief of pain, limiting the size of myocardial infarction, reducing mortality (1.5 million IU intravenously in 60 minutes)
3.Heparin intravenous bolus (if thrombolysis is not performed) Prevention or limitation of coronary thrombosis, prevention of thromboembolic complications, reduction of mortality (10000-15000 IU intravenous bolus)
4. Nitroglycerin or isosorbide dinitrate intravenously drip. Relief of pain syndrome, reduction in the size of myocardial infarction and mortality (10 mcg / min. with an increase in speed by 20 mcg / min every 5 minutes under the control of heart rate and blood pressure_
5. Beta blockers: propranolol (obzidan) Decreased myocardial oxygen demand, relief of pain, reduction of necrosis, prevention of ventricular fibrillation and left ventricular rupture, recurrent myocardial infarction, reduction of mortality (1 mg / min every 3-5 minutes up to a total dose of 10 mg)
6. Acetylsalicylic acid (aspirin) Relief and prevention of processes associated with platelet aggregation; with early (!) Appointment reduces mortality (160-325 mg chew;)
7. Magnesium sulfate (cormagnesin) Decrease in myocardial oxygen demand, relief of pain, reduction in the size of necrosis, prevention of cardiac arrhythmias, heart failure, reduction in mortality (1000 mg of magnesium (50 ml of 10%, 25 ml of 20% or 20 ml of 25% solution) intravenously for 30 minutes.)
Conducting a complete examination of a patient with suspected ACS at the prehospital stage is difficult due to lack of time, lack of necessary equipment, and the severity of the victim's condition. At the same time, the proposed algorithm is quite feasible, it is necessary for choosing the right treatment tactics, as well as for preparing the patient for therapy at the prehospital stage:
1. Determination of respiratory rate, heart rate, AT, blood saturation O 2 .
2. ECG registration in 12 leads.
3. ECG monitoring at the entire stage of treatment and transportation of the patient.
4. Ensure readiness for possible defibrillation and CPR.
5. Providing intravenous access.
6. Brief sighting history, physical examination (see Appendix 1).
Complaints. There are several options for the clinical onset of GCS:
Prolonged (more than 20 minutes) anginal pain at rest;
The occurrence of severe angina for the first time in life (III functional class according to the classification of the Canadian Society for Cardiovascular Diseases);
Recent destabilization of previously stable angina and elevation to at least functional class III (progressive angina)
Postinfarction angina.
Typical clinical symptom GCS - pain or heaviness behind the sternum, radiating to the left arm, neck or jaw, can be intermittent (usually lasts for several minutes) or sustained (more than 20 minutes), may be accompanied by sweating, nausea, abdominal pain, shortness of breath, fainting.
A prolonged attack of pain in the region of the heart is observed in 80% of patients (Fig. 3.2), the remaining variants of the development of GCS account for 20%.
Atypical variants of the course of GCS are quite common, manifested by pain in the epigastric region, dyspepsia, dagger-like chest pain, pleural pain, or increasing shortness of breath. In particular, these GCS variants are more often observed in young (25-40 years old) and elderly (over 75 years old) patients with diabetes mellitus, chronic kidney failure, dementia and women.
When collecting history diseases, it is necessary to establish the exact time from the onset of an attack of chest pain and its duration; the nature of pain, its localization and irradiation; previous attempts to relieve pain with nitroglycerin; conditions under which pain occurs, its connection with physical, psycho-emotional stress; the presence of attacks of pain or suffocation when walking, which forced them to stop, their duration in minutes, there was an effect of taking nitroglycerin; compare the intensity, frequency of occurrence, nature and localization of an anginal attack or suffocation with those sensations that arose earlier during exercise, exercise tolerance, or an increased need for nitrates.
Be sure to specify: medicines takes the patient daily; the patient took medicines before the arrival of BE (W) MD; presence of risk factors for cardiovascular disease arterial hypertension, smoking, diabetes mellitus, hypercholesterolemia) the presence of concomitant diseases: heart rhythm disturbance, cerebrovascular accident,
Rice. 3.2.
oncological diseases, peptic ulcer of the stomach and duodenum, blood diseases and the presence of bleeding in the past, operations, COPD, and the like; have allergic reactions to medications.
At physical examination there may be no changes. The basis for diagnosis and treatment may be symptoms of heart failure or hemodynamic disorders. An important goal of the physical examination is to rule out non-cardiac causes of heart pain, non-ischemic causes of heart disease (eg, thromboembolism). pulmonary artery, dissection of the aortic wall, pericarditis, valvular heart disease), identification of such possible extracardiac causes as acute illness lungs (pneumothorax, pneumonia or pleural effusion). The difference in AT on the upper and lower limbs, arrhythmic pulse, heart murmurs, pericardial rub, pain on palpation, masses in the abdominal cavity suggest other diagnoses.
A physical examination of the patient begins with an immediate assessment of the general condition and vital functions: consciousness, respiration, blood circulation according to the ABCDE algorithm, respectively, first of all, the identified violations must be eliminated. Perform visual color assessment skin, humidity, swelling of the jugular veins. Assess the state of the cardiovascular respiratory system patient (pulse, blood pressure, respiratory rate, auscultation of the heart and blood vessels, auscultation of the lungs).
Express registration of electrocardiogram (ECG) in 12 leads- this is the most diagnostic method that is used for suspected ACS, it must be carried out within the first 10 minutes after the arrival of the emergency carriage medical care. The ECG should be analyzed immediately or, in doubtful cases, the ECG signal should be sent to a telemetry advisory center for urgent interpretation issues (see Appendix 2).
Non-ST-elevation ACS is characterized by depression or transient ST-segment elevation and/or T-wave changes (Fig. 3.3). The presence of a sustained ST segment elevation (> 20 min) indicates the presence of GCS with ST segment elevation, is the equivalent of AMI, the treatment tactics of which are somewhat different (Fig. 3.4). During episodes of myocardial ischemia, a transient blockade of the legs of the bundle of His is sometimes observed, more often the left leg or its branches (Fig. 3.5).
Rice. 3.3.
Rice. 3.4.
Rice. 3.5.
It should be taken into account that the standard ECG at rest does not adequately reflect the dynamic nature of coronary thrombosis and myocardial ischemia. Almost 2/3 of episodes of the unstable phase are clinically asymptomatic and are not recorded on the ECG, however, this does not exclude the diagnosis of non-ST elevation ACS. Therefore, it is important to monitor or repeat the ECG at intervals of 20-30 minutes.
Level determination Cardiomarkers(troponin I and troponin T, CPK MB-fraction, Mioglobin) in the blood using a rapid diagnostic kit (Fig. 3.6).
At the prehospital stage, for emergency diagnosis, it is advisable to use a qualitative immunological test to determine the specific myocardial troponin T protein. In AMI, two rises in blood concentration are observed: after 2-3 hours and the maximum rise is observed after 8-10 hours. Normalization of the concentration of troponin in the blood occurs after 10-14 days. The method is simple, accessible, highly specific and allows diagnosing MI in the early and late periods of AMI - from 10 hours to 10 days (Fig. 3.7).
Rice. 3.6.
Rice. 3.7.
Cardiac troponins play a major role in diagnosis and risk stratification, and also differentiate between non-ST-elevation MI and unstable angina. In terms of specificity and sensitivity, troponins are superior to cardiac enzymes such as CPK (CPK), CPK MB fraction and myoglobin. An increase in the level of cardiac troponins reflects damage to cardiomyocytes, which in ACS without ST-segment elevation may be associated with distal embolization by platelet thrombi, which form in the area of rupture or erosion of an atherosclerotic plaque, an increase in the levels of fibrinogen and C-reactive protein (CRP) is also a risk factor in patients with OKS. The prognostic value of CRP is total in patients with myocardial injury. Troponin T and CRP are independent markers of cardiac death in long-term follow-up, but their prognostic value increases when they are measured together and also together with clinical markers.
The presence of symptoms of myocardial ischemia (chest pain, ECG changes and the appearance of asynergy of the heart wall), along with an increase in the level of troponins, is diagnostic criteria THEM. but negative result the test at the first study is not enough to rule out ACS without ST-segment elevation. Since in many patients the level of troponin increases after a few hours, if acute myocardial ischemia is suspected, a second analysis after 6-9 hours should be performed to verify the diagnosis.
First of all, it is necessary to take into account the presence of possible life-threatening diseases of other organs. In particular, pulmonary embolism may be accompanied by shortness of breath, chest pain and ECG changes, as well as an increase in the level of cardiac biomarkers. To exclude this disease, express diagnostics of the level of D-dimer is carried out. There may be other causes of non-coronary troponin elevation that are important for differential diagnosis. These include: chronic and acute renal dysfunction; acute and chronic severe congestive heart failure; hypertensive crisis; tachy or bradyarrhythmias; heavy pulmonary hypertension; inflammatory diseases heart (myocarditis, myopericarditis) acute neurological diseases (stroke, subarachnoid bleeding) aortic dissection, aortic valve insufficiency, hypertrophic cardiopathy; mechanical damage to the heart (contusion, ablation, stimulation, cardioversion, myocardial biopsy); hypothyroidism with takotsubo cardiomyopathy; systemic infiltrative diseases (amyloidosis, hemochromatosis, sarcoidosis, scleroderma) toxic effects of drugs (adriamycin, 5-fluorouracil, herceptin, poison) burns (> 30 % body surface) rhabdomyolysis; critically ill patients (respiratory failure or sepsis).
The choice of management strategy for patients with an established diagnosis of ACS determines the risk of disease progression to acute myocardial infarction and death. The key elements of risk assessment, in addition to age and previous history of coronary artery disease, are clinical examination, evaluation of ECG, biochemical parameters and the functional state of the left ventricle.
Step 1. Assess the severity of the condition and the risk of death
At this stage, it is necessary to collect an anamnesis and complaints of the patient. An anamnesis of the present disease, as well as concomitant and past diseases, is collected. Then the patient is examined with an assessment of the frequency of respiratory movements, auscultation of the lungs,The presence of peripheral edema and other signs of decompensation (enlarged liver, hydrothorax) is also checked.
Stage 2. Analysis of the electrocardiogram
ECG in acute coronary syndrome. Options for displacement of the ST segment in case of damage. There is a change or displacement of the ST segment, a change in the T wave.
Stage 3. Treatment of acute coronary syndrome at the prehospital stage
Principles of treatment at the prehospital stage:
- Adequate anesthesia
- Initial antithrombotic therapy
- Treatment of complications
- Fast and gentle transport to the medical facility
Anesthesia:
- nitroglycerin under control blood pressure
- intravenous analgin + diphenhydramine
- IV morphine 1% - 1.0 per 20.0 saline.
Possible complications:
-
- acute heart failure
Initial antithrombotic therapy in acute coronary syndrome
- Aspirin 1 tab. chew (with intolerance to clopidogrel 300 mg.)- Heparin 5 thousand units. (by doctor's prescription).
Emergency hospitalization in the intensive care unit: for thrombolytic therapy (introduction of streptokinase, streptodecase), as well as to resolve the issue of coronary angiography and balloon coronary angioplasty
Vertkin A.L., Moshina V.A., Topolyansky A.V., M.A. Malsagov
Department of Clinical Pharmacology (Head - Prof. Vertkin A.L.) of the Moscow State University of Medicine and Dentistry (Rector - Academician of the Russian Academy of Medical Sciences Yushchuk N.D.), National Scientific and Practical Society for Emergency Medicine
Modern management of patients with acute ischemic myocardial injury is based on the pathogenesis and morphology of coronary heart disease (CHD). The morphological substrate of IHD is an atherosclerotic plaque, the state of which largely determines the clinical variants of the disease: unstable angina, myocardial infarction with a Q wave and myocardial infarction without a Q wave. Since in the first hours (and sometimes days) from the onset of the disease, it can be difficult to differentiate acute infarction myocardial infarction and unstable angina, to designate the period of exacerbation of coronary artery disease, the term "acute coronary syndrome" (ACS) has recently been used, which is understood as any group of clinical signs that make it possible to suspect myocardial infarction or unstable angina. ACS is a term that is valid at the first contact between a doctor and a patient, it is diagnosed on the basis of pain syndrome (prolonged anginal attack, first-time progressive angina pectoris) and ECG changes, and therefore is especially suitable for the pre-hospital diagnosis and treatment of IHD destabilization.
The relevance of creating balanced and carefully substantiated recommendations for emergency care physicians on the treatment of ACS is largely due to the prevalence of this pathology. As you know, in this Russian Federation, the daily number of EMS calls is 130,000, including those for ACS from 9,000 to 25,000.
Scope and adequacy emergency care in the first minutes and hours of the disease, i.e. at the prehospital stage largely determines the prognosis of the disease. There are ACS with ST-segment elevation or acute complete blockade of the left bundle branch block and without ST-segment elevation. A high risk accompanies ACS with ST segment elevation; these patients are indicated for thrombolytic therapy and, in some cases, hospitalization with the possibility of cardiac surgery. It is known that the earlier reperfusion therapy with the use of thrombolytic drugs is carried out, the higher the chances of a favorable outcome of the disease. Moreover, in accordance with the data obtained in the CAPTIM study (2003), the results of early initiation of thrombolytic therapy (TLT) in the prehospital stage are comparable in effectiveness to the results of direct angioplasty and exceed the effectiveness of treatment initiated in the hospital. This allows us to consider that in Russia the damage from the impossibility of widespread distribution surgical methods revascularization in ACS (primarily economic reasons) can be partially compensated by the earliest possible start of TLT.
For the success of TLT therapy in ACS with ST segment elevation, the most important role is played by its early start - optimally, within 1 hour after the onset of pain. It is no coincidence that the standard of care for patients with ACS in the UK is TLT within 1 hour from the onset of symptoms (Department of Health. National Service Framework for coronary heart disease. 2000).
In the clinical guidelines developed by the working group of the European Society of Cardiology and the European Council for Resuscitation for the treatment of acute heart attacks at the prehospital stage, TLT is recommended if there are local programs for prehospital thrombolysis, if there are qualified personnel at the stage of prehospital treatment, in a different situation - in case of delay with transportation for more than 30 minutes or delay in reperfusion therapy in the hospital for more than 60 minutes. The American College of Cardiology, in conjunction with the American Heart Association, have categorized recommendations for the prehospital use of thrombolytics as low-evidence-based recommendations and provide for the use of thrombolytic agents in situations where the expected loss of time to transport a patient is more than 90 minutes.
Thus, the need for TLT therapy at the prehospital stage is determined mainly by the time from the onset of ACS symptoms to the start of therapy. According to Dracup K. et al., 2003, this delay ranges from 2.5 hours in England to 6.4 hours in Australia in different countries. The delay in therapy is most often observed in the development of ACS in women, the elderly, with the development of ACS against the background of diabetes, atrial fibrillation, as well as in the evening and at night (Berton G. et al., 2001, Gurwitz J. H. et al., 1997, Kentsch M. et al., 2002). The time from the onset of ACS symptoms to the start of therapy is largely determined by population density, the nature of the area (urban, rural), living conditions, etc. (Bredmose PP, et al., 2003, Ottesen MM et al., 2003, Vertkin A. L, 2004).
According to the results of our study, in Russia, at the prehospital stage with ACS with an elevation of the S segment TLT, TLT is performed in less than 20% of cases, including in the metropolis in 13%, in medium-sized cities - in 19%, in rural areas - in 9 % (Vertkin A.L., 2003). The frequency of TLT does not depend on the time of day and season, but the time of calling the EMS is delayed by more than 1.5 hours, and in rural areas - by 2 hours or more. The time from the onset of pain to the “needle” averages 2 to 4 hours and depends on the location, time of day and season. The gain in time is especially noticeable in large cities and rural areas, at night and in the winter season. The conclusions of our work indicate that prehospital thrombolysis allows to achieve a decrease in mortality (13% with prehospital thrombolysis, 22.95% with inpatient thrombolysis), the incidence of postinfarction angina pectoris without a significant impact on the incidence of recurrence of myocardial infarction and the appearance of signs of heart failure. .
According to the recommendation of the ACA / AHA (2002), the treatment of ACS involves the use of nitroglycerin to relieve pain, reduce preload and myocardial oxygen demand, limit the size of myocardial infarction, as well as to treat and prevent complications of myocardial infarction. The recommendations developed by the working group of the European Society of Cardiology and the European Council for the Resuscitation of Acute Heart Attacks in the prehospital stage do not recommend the widespread use of nitrates, but their use in persistent pain or the presence of heart failure is recognized as justified.
Relief of pain in ACS begins with sublingual administration of nitroglycerin (0.4 mg in aerosol or tablets). In the absence of effect from sublingual administration of nitroglycerin (three doses with breaks of 5 minutes), therapy with narcotic analgesics is indicated. It should be noted that there have been no serious studies of the effectiveness of nitrates in non-ST elevation ACS on the ECG, especially since there has not been a comparative study of the effectiveness of various dosage forms nitroglycerin. Nitroglycerin is available in five main forms: sublingual tablets, tablets for oral intake, spray/aerosol, transdermal (buccal) and intravenous. When providing emergency care, aerosol forms (nitroglycerin spray), tablets for sublingual use and solution for intravenous infusion are used.
The advantages of nitroglycerin in the form of a spray over other forms include the speed of relief of an angina attack (the absence of essential oils, slowing down absorption, provides a faster effect); dosing accuracy (when you press the canister valve, an exactly set dose of nitroglycerin is released); ease of use; safety and preservation of the drug due to special packaging (nitroglycerin is an extremely volatile substance); long shelf life (up to 2 years) compared to the tablet form (up to 3 months after opening the package); equal efficacy with fewer side effects compared to parenteral forms; the possibility of using with difficult contact with the patient and in the absence of consciousness; the possibility of use in elderly patients suffering from a decrease in salivation. In addition, from the point of view of pharmacoeconomics, the use of a spray is also more justified: one package can be enough for 40-50 patients, while intravenous administration is technically more difficult and requires an infusion system, a solvent, a venous catheter, and the drug itself.
In our study, a comparative evaluation of the efficacy and safety of the use of nitroglycerin in the form of an aerosol (123 patients) or intravenous infusion (59 patients) was carried out in non-ST elevation ACS. The clinical condition, the presence of pain syndrome, blood pressure and heart rate, ECG at baseline and 15, 30 and 45 minutes after parenteral or sublingual administration of nitrates were assessed. Undesirable effects were also monitored medicines. In addition, a 30-day prognosis in patients was assessed: mortality, the incidence of Q-myocardial infarction in patients with initial non-ST elevation ACS.
During therapy with nitroglycerin in the form of a spray, after 15 minutes, the pain syndrome was stopped in 82.1% of patients, after 30 minutes - in 97.6%, and after 45 minutes - in all patients of this group. Against the background of intravenous administration of nitroglycerin, after 15 minutes the pain was relieved in 61% of patients, after 30 minutes - in 78%, after 45 minutes - in 94.9% of patients. It is very important that the frequency of recurrence of the pain syndrome was equally low in both groups.
The use of nitroglycerin in both groups led to a significant decrease in the level of SBP, and in patients who received nitroglycerin per os, an insignificant decrease in the level of DBP. Patients treated with nitroglycerin infusion experienced a statistically significant reduction in DBP. There were no statistically significant changes in heart rate. As expected, infusion administration of nitroglycerin was accompanied by a significantly higher incidence of side effects associated with a decrease in blood pressure (8 episodes of clinically significant arterial hypotension), however, all these episodes were transient and did not require the appointment of vasopressor agents. In all cases of hypotension, it was enough to stop the infusion and after 10-15 minutes the blood pressure returned to an acceptable level. In two cases, continued infusion at a slower pace again led to the development of hypotension, which required the final withdrawal of nitroglycerin. With sublingual use of nitroglycerin, hypotension was noted only in two cases.
Against the background of nitrate therapy, hyperemia of the face was detected when using a spray in 10.7%, with intravenous infusion of nitroglycerin - in 12% of cases; tachycardia - in 2.8% and 11% of cases, respectively, headache with sublingual administration of the drug was noted in 29.9% of cases, and with intravenous administration in 24% of cases.
Thus, in patients with ACS without ST elevation, sublingual forms of nitroglycerin are not inferior in analgesic effect to parenteral forms; side effects in the form of arterial hypotension and tachycardia with intravenous administration of nitroglycerin occur more often than with sublingual administration, and facial flushing and headache occur with intravenous administration with the same frequency as with sublingual administration. All this makes it possible to consider the optimal use of nitroglycerin in the form of a spray as an antianginal agent in the treatment of ACS as at the prehospital stage.
The results of our studies and analysis of data available in the literature, existing clinical guidelines allowed us to develop the following algorithm for managing a patient with ACS at the prehospital stage.
Algorithm for managing a patient with ACS at the prehospital stage
Bibliography:
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