Acute coronary syndrome: emergency medical care at the prehospital stage. Symptoms and emergency care in Acute Coronary Oaks Syndrome prehospital emergency care

Carrying out a full examination of a patient with suspected ACS at the prehospital stage is difficult due to the 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 to select the correct treatment tactics, as well as to prepare the patient for therapy at the pre-hospital stage:

1. Determination of RR, HR, AT, blood saturation O 2.

2. Registration of ECG in 12 leads.

3. Monitoring of the ECG at all stages of treatment and patient transportation.

4. Ensuring preparedness for possible defibrillation and CPMR.

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 min) anginal pain at rest;

The emergence for the first time in life of severe angina (III functional class according to the classification of the Canadian Society of Cardiovascular Diseases);

Recent destabilization of pre-stable angina pectoris and elevation to at least functional class III (progressive angina pectoris)

Postinfarction angina.

Typical clinical symptom GCS - pain or heaviness behind the sternum, radiating to the left arm, neck or jaw, can be intermittent (usually last for several minutes) or persistent (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, they are manifested by pain in the epigastric region, dyspepsia, dagger-like chest pain, pleural pain or increasing shortness of breath. In particular, these variants of GCS are more often observed in young (25-40 years old) and elderly (over 75 years old) patients with diabetes mellitus, chronic renal failure, dementia and women.

When collecting anamnesis disease, 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 bouts of pain or suffocation when walking, which forced 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: the patient takes medications daily; the patient took medications before the arrival of BY (W) MD; the presence of risk factors for cardiovascular diseases ( arterial hypertension, smoking, diabetes mellitus, hypercholesterolemia) the presence of concomitant diseases: heart rhythm disturbance, cerebrovascular accident,

Figure: 3.2.

oncological diseases, gastric ulcer and duodenal ulcer, blood diseases and the presence in the past of bleeding, operations, COPD and the like; have allergic reactions to medications.

When physical examination there may be no changes. Symptoms of heart failure or hemodynamic disturbances may be the basis for diagnosis and treatment. An important goal of the physical examination is to rule out noncardiac causes of heart pain that are not ischemic in nature (such as thromboembolism pulmonary artery, dissection of the aortic wall, pericarditis, valvular heart disease), identification of possible extracardiac causes such as acute lung disease (pneumothorax, pneumonia or pleural effusion). Difference AT on top and lower limbs, arrhythmic pulse, heart murmurs, pericardial friction murmur, pain on palpation, formation in abdominal cavity suggest other diagnoses.

Begin the physical examination of the patient with an immediate assessment general condition and vital functions: consciousness, respiration, blood circulation according to the ABCDE algorithm, respectively, first of all it is necessary to eliminate the identified violations. A visual assessment of the color of the skin, moisture, swelling of the cervical veins is carried out. The state of the patient's cardiovascular and respiratory systems is assessed (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 very method of diagnostics that is used when an ACS is suspected; it must be carried out within the first 10 minutes after the arrival of the emergency medical carriage. The ECG should be analyzed immediately or, in doubtful cases, the ECG signal should be sent to an advisory telemetry center for urgent interpretation issues (see Appendix 2).

ACS without ST-segment elevation is characterized by depression or short-term elevation of the ST segment and / or changes in the T wave (Fig. 3.3). The presence of stable ST-segment elevation (\u003e 20 min) indicates the presence of GCS with ST-segment elevation, is equivalent to AMI, the treatment tactics of which are somewhat different (Fig. 3.4). In episodes of myocardial ischemia, transient blockade of the bundle branch, more often the left leg or its branches, is sometimes observed (Fig. 3.5).

Figure: 3.3.

Figure: 3.4.

Figure: 3.5.

It should be borne in mind that a standard resting ECG does not adequately reflect the dynamic nature of coronary thrombosis and myocardial ischemia. Almost 2/3 of cases of unstable phase episodes are clinically asymptomatic and are not recorded on the ECG, however, this does not exclude the diagnosis of ACS without ST segment elevation. Therefore, it is important to monitor or repeat the ECG at intervals of 20-30 minutes.

Determination of the level of Cardiomarkers (troponin I and troponin T, MB-fraction of CPK, Mioglobin) in the blood using a kit for express diagnostics (Fig. 3.6).

At the prehospital stage, for emergency diagnostics, it is advisable to use a qualitative immunological test to determine the specific myocardial protein troponin T. With AMI, two rises are observed, an increase in blood concentration: after 2- 3 hours and the maximum rise is observed after 8-10 hours. The normalization of the concentration of troponin in the blood occurs after 10-14 days. The method is simple, accessible, highly specific and allows diagnosing myocardial infarction in the early and late stages of AMI - from 10 hours to 10 days (Fig. 3.7).

Figure: 3.6.

Figure: 3.7.

Cardiac troponins play a major role in the diagnosis and risk stratification and can also differentiate non-ST-segment elevation MI and unstable angina. In terms of specificity and sensitivity, troponins are superior to cardiac enzymes such as CPK (CPK), MV fraction of CPK 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, formed in the area of \u200b\u200brupture 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. Predictive value of CRP in total in patients with myocardial injury. The concentration of troponin T and CRP are independent markers of cardiac death during long-term follow-up, but their predictive value increases when they are jointly determined, as well as 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 troponin levels are diagnostic criteria for MI. However, a negative test result in the first study is not enough to exclude 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 should be carried out after 6-9 hours 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 increased cardiac biomarkers. To exclude this disease, express diagnostics of the D-dimer level is performed. There are other possible causes of non-coronary elevation of troponin levels, which are important for differential diagnosis. These include: chronic and acute renal dysfunction; severe and chronic congestive heart failure; hypertensive crisis; tachy or bradyarrhythmias; severe pulmonary hypertension; inflammatory diseases heart (myocarditis, myopericarditis) acute neurological diseases (stroke, subarachnoid bleeding) aortic dissection, deficiency aortic valve, hypertrophic cardiopathy; mechanical damage heart (contusion, ablation, pacing, cardioversion, myocardial biopsy) hypothyroidism with takotsubo cardiomyopathy; systemic infiltrative diseases (amyloidosis, hemochromatosis, sarcoidosis, scleroderma) toxic effects of drugs (adriamycin, 5-fluorouracil, herceptin, poison) burns (\u003e 30 % body surface) rhabdomyolysis; critically ill patients (respiratory distress or sepsis).

The choice of management strategy for patients with an established ACS diagnosis 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 heart disease, are clinical examination, ECG assessment, biochemical parameters and functional state of the left ventricle.

ACS treatment at the prehospital stage: modern performance Prof. Tereshchenko S. N. Institute of Clinical Cardiology. A. L. Myasnikova. RKNPK Russian Cardiology Research and Production Complex

Acute coronary syndrome One cause of disease but other clinical manifestations and other treatment strategies Retrosternal pain Acute coronary syndrome No ST elevation No troponin Unstable angina ST elevation Troponin position MV CK MI without ST elevation ST elevation MI

Pathogenesis of acute coronary syndrome Rupture of a vulnerable atherosclerotic plaque intracoronary thrombosis change in the geometry of the plaque distal embolization local spasm Spasm of the coronary artery at the site of stenosis without visible stenosis of myocardial oxygen demand with significant stenosis of oxygen delivery to the myocardium in case of significant stenosis Development / aggravation of acute symptoms coronary syndrome)

Treatment goals for acute coronary syndrome Improve mortality prognosis, frequency of MI complications Eliminate symptoms and syndromes pain HF arrhythmias ...

The main tasks for the first inspection § emergency care § Evaluation of the presumptive cause of chest pain (ischemic or non-ischemic). § Evaluation of the immediate risk of life-threatening conditions. § Determination of the indication and location of hospitalization.

Physician's tactics for ACS at the prehospital stage. § Initial assessment of patients with chest pain. Differential diagnosis.

Differential diagnosis of chest pain is not only a clinical, but also an organizational problem solved in the diagnostic departments for patients with chest pain

DOCTOR'S TACTICS IN ACS AT THE PREHOSPITAL STAGE § Initial assessment of patients with chest pain. Differential diagnosis. § Indication for hospitalization and transportation.

The slightest suspicion (probable ACS) regarding the ischemic genesis of chest pain, even in the absence of characteristic electrocardiographic changes, should be the reason for the immediate transportation of the patient to the hospital.

DOCTOR'S TACTICS IN ACS AT THE PREHOSPITAL STAGE § Initial assessment of patients with chest pain. Differential diagnosis. § Indication for hospitalization and transportation. §Prehospital assessment of the risk of death and development of AMI in patients with ACS without ST segment elevation.

Risk stratification in ACS without ST Acute risk of adverse outcomes in ACS without ST (assessed by follow-up) High recurrent angina dynamic displacements of the ST segment (the more common, the worse the prognosis) Low during follow-up ischemia does not recur no ST segment depression early postinfarction angina is not markers myocardial necrosis cardiac troponins (the higher, the worse the prognosis) normal cardiac troponin levels when measured twice with an interval of at least 6 hours diabetes mellitus hemodynamic instability severe arrhythmias Eur Heart J 2002; 23: 1809 -40

DOCTOR'S TACTICS IN ACS AT THE PREHOSPITAL STAGE § Initial assessment of patients with chest pain. Differential diagnosis. § Indication for hospitalization and transportation. §Pre-hospital assessment of the risk of death and MI in patients with ACS. § Treatment of USC at the prehospital stage.

Providing emergency care Anesthesia Nitroglycerin 0.4 mg p / i or spray with. BP\u003e 90 If ineffective, after 5 minutes Nitroglycerin 0.4 mg p / i or spray with. BP\u003e 90 With ineffectiveness "03" Morphine (especially with excitement, acute heart failure) IV 2 -4 mg + 2 -8 mg every 5 -15 minutes or 4 -8 mg + 2 mg every 5 minutes or 3 - 5 mg before pain relief IV nitroglycerin with blood pressure\u003e 90 mm Hg, if there is pain, acute pulmonary congestion, high blood pressure

Basic principles of treatment of patients with ACS without ST segment elevation at the prehospital stage §Adequate pain relief §Antithrombotic therapy.

Influence of aspirin and heparin on the sum of deaths and myocardial infarction in ACS without ST Meta-analysis of conducted studies% p \u003d 0, 0005 12, 5 6, 4 5, 3 2, 0 n \u003d 2488 No treatment www. acc. org n \u003d 2629 Aspirin 5 days-2 years Heparin 1 week

Factors influencing the choice of antithrombotic treatment for ACS without persistent ST The nature of myocardial ischemia and the time of the last episode Risk of poor outcome (MI, death) in the near future Approach to patient management invasive conservative Risk of bleeding Renal function Clinical judgment on the presence of ongoing intracoronary thrombosis

Aspirin for ACS without ST. Current recommendations Initial dose European Society of Cardiology, ACS without ST (2002) Long-term use 75 -150 ≤ 100 with clopidogrel Class I (A) American College of Cardiology and Heart Association, ACS without ST (2002) 162 -325 75 - 160 I (A) Russian recommendations, ACS without ST (2004) 250 -500 75 -325, then 75 -160 (150) - European Society of Cardiology, antiplatelet agents (2004) 160 -300 75 -100 I (A ) American College of Thoracic Physicians (2004) 160 -325 75 -162 I (A) Eur Heart J 2002; 23: 809 -40. Circulation 2002; 106: 893 -1900. Chest 2004; 126: 513 S-548 S. Eur Heart J 2004; 25: 166 -81. Cardiology 2004, supplement.

Heparin in ACS without persistent ST on ECG 48 -72 h from pain IV infusion of UFH SC injections of LMWH Observation 6-12 hours High risk of thrombotic complications No evidence of high risk of thrombotic complications ST troponin ... no ST normal troponin (twice with an interval \u003e 6 hours) Administration from 2 to 8 days (by doctor's decision) Cancellation of heparin

Clopidogrel addition in ACS without ST CURE study (n \u003d 12 562) C-c death, MI, stroke, severe ischemia risk 34% р \u003d 0, 003 11, 4% 0, 14 Risk of event 0, 12 Heparin in 92%, of which LMWH 54% Aspirin 0, 10 9, 3% 0, 08 Aspirin + clopidogrel 0, 06 0, 04 Hours after randomization 0, 02 0, 00 0 Circulation 2003; 107: 966 - 72 3 6 9 12 Months

Manifestations of myocardial ischemia Severe pain behind the sternum squeezing, pressing Sweat, sticky cold sweat Nausea, vomiting Shortness of breath Weakness, collapse

Clinical variants of MI% 65, 6 status anginosus 89 status asthmaticus 7 10, 5 status gastralgicus 1 6, 7 arrhythmic 2 14, 3 cerebral 1 - asymptomatic - 2, 9 616 people 105 people Syrkin A.L.

Necessary and sufficient signs for the diagnosis of AMI One of the following criteria is sufficient for the diagnosis of AMI: - the clinical picture of ACS; - the appearance of pathological Q waves on the ECG; - ECG changes, indicating the appearance of myocardial ischemia: the occurrence of elevation or depression of the ST segment, blockade of LPH;

50% of deaths from UTI. ST occurs in the first 1, 5-2 hours from the onset of an anginal attack and most of these patients die before the arrival of the ambulance team. Therefore, the greatest efforts should be made so that first aid is provided to the patient as early as possible, and that the volume of this aid is optimal.

Organization of EMS work in AMI Treatment of a UTI patient. ST is a single process that begins in the prehospital phase and continues in the hospital. For this, the ambulance teams and hospitals where patients with ACS are admitted must work according to a single algorithm based on common principles of diagnosis, treatment and a common understanding of tactical issues § Two-stage system, when, upon suspicion of myocardial infarction, the linear ambulance team calls on itself a "specialized" which actually begins treatment and transports the patient to the hospital, leads to an unjustified loss of time §Each ambulance team (including the paramedic) must be ready to active treatment patient with UTI. ST

Organization of EMS work in AMI. cardiac arrhythmias or acute heart failure - the necessary therapy, including measures for cardiopulmonary resuscitation § Emergency medical service teams in each locality should have clear instructions to which hospitals it is necessary to transport UTI patients. ST or suspected UTI. ST § Doctors of these hospitals provide emergency medical services with appropriate advice if necessary

It is necessary to transport the patient as soon as possible to the nearest specialized institution, where the diagnosis will be clarified and treatment will continue

Linear ambulance team should be equipped with the necessary equipment 1. Portable ECG with autonomous power supply; 2. Portable device for EIT with autonomous power supply with heart rate control; 3. Set for cardiopulmonary resuscitation, including a device for manual ventilation; 4. Equipment for infusion therapyincluding infusomats and perfusers; 5. Set for the installation of an IV catheter; 6. Cardioscope; 7. Pacemaker; 8. System for remote ECG transmission; 9. Mobile communication system; 10. Suction; 11. Medicines required for basic therapy of AMI

Treatment of uncomplicated UTI. ST at the prehospital stage Each ambulance team (including the paramedic) should be ready to actively treat the patient with UTI. ST Basic therapy. 1. Eliminate pain syndrome. 2. Chew a tablet containing 250 mg ASA. 3. Take 300 mg of clopidogrel by mouth. 4. Start IV infusion of NG, primarily with persisting angina pectoris, AH, AHF. 5. Start treatment with b-blockers. Preferably the initial intravenous administration, especially with ischemia, which persists after intravenous administration of narcotic analgesics or recurs, hypertension, tachycardia or tachyarrhythmia, without HF. It is planned to perform primary TBA. The loading dose of clopidogrel is 600 mg.

Oxygen therapy In all cases, 2 l / min through nasal catheters in the first 6 h

Nitrates in acute myocardial infarction Indications for the use of nitrates § myocardial ischemia § acute congestion in the lungs § need for blood pressure control No contraindications § p. BP 30 mm Hg below baseline § HR 100 § Suspected right ventricular MI §

Prehospital triple antiplatelet therapy On-TIME 2 trial data Prehospital IH IIb / IIIa tirofiban (bolus 25 mcg / kg followed by 0.15 mcg / kg / min infusion for 18 hours) or placebo in addition to aspirin (500 mg IV), clopidogrel (600 mg PO) and IV bolus (5000 IU) UFH p \u003d 0.043 p \u003d 0.051 p \u003d 0.581

Restoration of coronary perfusion The mainstay of treatment for acute MI is restoration of coronary blood flow - coronary reperfusion. The destruction of the thrombus and the restoration of myocardial perfusion lead to limiting the extent of its damage and, ultimately, to an improvement in the short and long term prognosis. Therefore, all patients with UTI. ST should be examined without delay to clarify the indications and contraindications for the restoration of coronary blood flow. Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST-segment elevation ECG. 2007 VNOK

Thrombolytic therapy in patients with AMI in 2008 according to 12 regions 2008

Prehospital thrombolysis: gain in time \u003d saving the myocardium Decision to call an ambulance Ambulance arrival Arrival to the hospital Occurrence of pain Diagnosis Clearance in the emergency room Actilize SK today PTCA Metallize in ICU tomorrow Occurrence of pain The decision to call an ambulance in Metalysis at the Arrival Pre-hospital emergency diagnosis Early thrombolysis strategy

Prehospital thrombolysis for STEMI

USIC 2000 Register: Reducing Mortality in Prehospital Thrombolysis Mortality (%) 15 12. 2 10 5 8. 0 6. 7 3. 3 0 Dogosp. TL TL in hospital Without PCI of reperfusion therapy Danchin et al. Circulation 2004; 110: 1909-1915.

VIENNA STEMI REGISTRY: Change in reperfusion strategy Thrombolysis Without reperfusion PCI 60 60 50 50 Patients (%) 40 34 26.7 30 20 16 13.4 10 0 VIENNA 2002 VIENNA 2003/2004 Kalla et al. Circulation 2006; 113: 2398-2405.

VIENNA STEMI REGISTRY: Time from disease onset to treatment with different strategies 0 -2 h 100 90 19.5 6 -12 h 2 -6 h 5.1 80 44.4 Patients (%) 70 60 50 65.9 40 30 20 10 50.5 14.6 0 PCI THROMBOLYSIS Kalla et al. Circulation 2006; 113: 2398-2405.

GRACE REGISTRY Reperfusion therapy No reperfusion PCI only 50 48 Patients (%) 43 40 40 41 36 32 30 35 33 33 31 30 25 20 10 TLT only 35 32 26 19 13 15 0 1999 2000 2001 2002 Years 2003 2004 Eagle et al. 2007, Submitted

Treatment of uncomplicated UTI. ST at the prehospital stage Thrombolytic therapy at the prehospital stage. It is carried out in the presence of indications and the absence of contraindications. When using streptokinase, at the discretion of the physician, direct-acting anticoagulants can be used as concomitant therapy. If anticoagulant use is preferred, UFH, enoxaparin, or fondaparinux may be chosen. When using fibrin-specific thrombolytics, enoxaparin or UFH should be used. Reperfusion therapy is not expected. The decision on the advisability of using direct anticoagulants may be postponed until admission to the hospital. Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST-segment elevation ECG. 2007 VNOK

Indications for TLT If the time from the onset of an anginal attack does not exceed 12 hours, and the ECG shows an elevation of the ST segment ≥ 0.1 m. V, at least in 2 consecutive chest leads or in 2 limb leads, or blockade of LPH appears. The introduction of thrombolytics is justified at the same time when ECG signs true posterior MI (high R waves in the right precordial leads and depression of the ST segment in leads V 1 -V 4 \u200b\u200bwith an upward T wave). Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST-segment elevation ECG. 2007 VNOK

Contraindications for TLT Absolute contraindications for TLT § Previous hemorrhagic stroke or CCD of unknown etiology; § ischemic stroke suffered within the last 3 months; § brain tumor, primary and metastatic; § suspicion of aortic dissection; § the presence of signs of bleeding or hemorrhagic diathesis (with the exception of menstruation); § significant closed injuries heads in the last 3 months; § changes in the structure of cerebral vessels, for example, arteriovenous malformation, arterial aneurysms Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST-segment elevation ECG. 2007 VNOK

Checklist for making a decision by the medical and paramedic team of the ambulance service to conduct a patient with acute coronary syndrome (ACS) TLT Check and mark each of the indicators given in the table. If all the boxes in the "Yes" column are marked and none in the "No" column, then thrombolytic therapy is indicated to the patient. If there is even one unmarked box in the “Yes” column, TLT therapy should not be performed and the checklist can be stopped. "Yes" The patient is oriented, can communicate Pain syndrome characteristic of ACS and / or its equivalents lasting at least 15-20 minutes. , but no more than 12 hours After the disappearance of the pain syndrome characteristic of ACS and / or its equivalents, no more than 3 hours have passed.Quality registration of ECG in 12 leads was performed.The doctor / paramedic of the EMS has experience in assessing changes in the ST segment and blockade of the bundle of His bundle on the ECG (test only in the absence of a remote ECG assessment by a specialist) There is a ST segment elevation of 1 mm or more in two or more adjacent ECG leads or a left bundle branch block is registered, which the patient did not have before The doctor / paramedic of the emergency medical service has experience in TLT Transportation of the patient to the hospital will take more than 30 minutes. It is possible to receive medical recommendations from a cardioreanimatologist of the hospital in real time. During the patient's transportation, there is a possibility of continuous monitoring of the ECG (at least in one lead), intravenous infusion (in "No"

Age over 35 for men and over 40 for women Systolic blood pressure does not exceed 180 mm Hg. Art. Diastolic blood pressure does not exceed 110 mm Hg. Art. The difference in systolic blood pressure levels measured on the right and left hand does not exceed 15 mm Hg. Art. There is no history of stroke or other organic (structural) brain pathology. clinical signs bleeding of any localization (including gastrointestinal and urogenital) or manifestations hemorrhagic syndrome In the submitted medical documents, there is no data on the patient's prolonged (more than 10 minutes) cardiopulmonary resuscitation or on the presence of internal bleeding in the last 2 weeks; the patient and his relatives confirm this. In the submitted medical documents there is no data on the transferred over the last 3 months. surgery (including on the eyes using a laser) or serious injury with hematomas and / or bleeding, the patient confirms this The submitted medical documents do not contain data on the presence of pregnancy or the terminal stage of any disease and the survey and examination data confirm this The submitted medical documents do not contain data on the presence of jaundice, hepatitis, renal failure and the data of the survey and examination of the patient CONCLUSION: TLT is CONTRAINDICATED to the patient, confirm this _______________ (full name) SHOWN (circle the necessary, cross out the unnecessary) The sheet was filled out: Doctor / paramedic (circle the necessary) _____________ (full name) Date ______ Time _____ Signature _______ to the patient in the checklist before hospital and filed in the medical history

Thrombolytic drugs Intravenous 1 mg / kg body weight (but not more than 100 mg): bolus 15 mg; subsequent infusion of 0.75 mg / kg of body weight in 30 minutes (but not more than 50 mg), then 0.5 mg / kg (but not more than 35 mg) in 60 minutes (total duration of infusion is 1.5 hours). Intravenous: bolus 2,000,000 IU and Purolaza followed by 4,000,000 IU infusion over 30-60 minutes. Streptokinase Intravenous infusion of 1,500,000 IU over 30-60 minutes). Tenecteplase Intravenous bolus: 30 mg at a weight of 90 kg. segment ST ECG. 2007 VNOK Alleplaza

Evolution of thrombolysis First generation Streptokinase allergenic, non-selective to fibrin Second generation Third generation Metalysis Equivalent to Alteplase Actilize High "gold standard" fibrin selectivity Fibrin-specific non-allergenic Continuous intravenous infusion Single bolus 5-10 seconds

Reducing the relative risk Meta-analysis of studies with early IV administration of beta-blockers for MI (n \u003d 52 411) 0 -5 -10 -15 -20 -13%

BETA-BLOCKERS: APPLICATION IN PATIENTS WITH ACS IN 59 RUSSIAN CENTERS GRACE register data (2000 -1) 100% N \u003d 2806 C ST - 50.3% Without ST - 49.7% 1 Prev. 7 days 3 During hospitalization 2 First 24 hours. 4 Recommended at discharge 100% Without ST C ST 55.6 54.3 50.7 50% 54 50% 20. 2 0% 4.3% 2.9 I / O 60.3 54.5 12.2 0% 1 2 3 4 I / O 1 2 3 4 www. cardiosite. ru

Intravenous administration of beta-blockers in acute myocardial infarction From the first hours / day To eliminate symptoms § persistence of ischemia § tachycardia without heart failure § tachyarrhythmia § blood pressure All without contraindications § expediency of intravenous infarction is discussed § if there are no contraindications

Beta-blockers for UTI. ST Drug Dose Treatment on the 1st day of the disease Metoprolol IV, 5 mg 2-3 times with an interval of at least 2 minutes; First oral administration 15 minutes after intravenous administration. Propronolol V / in 0.1 mg / kg for 2-3 doses at intervals of at least 2-3 minutes; First oral administration 4 hours after intravenous administration. Esmolol IV infusion at an initial dose of 0.05-0.1 mg / kg / min, followed by a gradual increase in the dose by 0.05 mg / kg / min every 10-15 minutes until an effect or dose of 0.3 mg / kg is achieved / min; for a more rapid onset of the effect, an initial administration of 0.5 mg / kg for 2–5 minutes is possible. Emolol is usually canceled after the second dose of an oral β-blocker, if the correct heart rate and blood pressure were maintained during their combined use.

ACS P ST Data at admission to hospital Odds ratio (confidence interval) HKB # 29 (n \u003d 58) Other centers (n \u003d 1917) Time from symptom onset to hospitalization (hours) 5, 48 2, 83 ST elevations on baseline ECG (%) 86, 2 93, 8 2.45 (1.13 -\u003e 5) Negative T on baseline ECG (%) 3.45 1.73 0.79 (0.12 -2.11) GRACE scale: proportion patients at risk of death \u003d 10% 10.3 19.4 2.08 (0.89 -4.88) Killip class I-II (%) 93.193.1 0.999 (0.35 -2.78 ) III (%) 5, 17 3, 86 0.74 (0.23 -2.41) IV (%) 02, 74 1.81 (0.25 -13.3) RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD )

ACS P ST Primary reperfusion therapy and anticoagulant treatment Odds ratio (confidence interval) GKB # 29 (n \u003d 58) Other centers (n \u003d 1917) 27, 6 75, 7 0 47, 9 Streptokinase (%) 24, 1 5, 0 0.17 (0.09 -0. 31) T-PA (%) 3, 5 22, 8\u003e 5 81, 0 94, 0 3.69 (1.86 -\u003e 5) LMWH (%) 0 62 , 4 UFH (%) 100 50.5 Fondaparinux (%) 0 0, 1 Bivalirudin (%) 0 0, 1 Primary reperfusion (%) Primary PCI (%) TLT: Anticoagulants (%) RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD)

Practical approaches in the treatment of AMI Within 10 - 15 minutes Emergency treatment § morphine 2-4 mg i.v. to effect -8 L / min for O 2 saturation\u003e 90% § § § Aspirin (if not given earlier): § § Clopidogrel 300 mg, chew 250 mg, 300 mg in suppository or 500 mg IV, age 90, if pain is present, acute congestion in the lungs, high blood pressure § solution of the issue of TLT !!!

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STATE AUTONOMOUS PROFESSIONAL EDUCATIONAL INSTITUTION OF THE REPUBLIC OF BASHKORTOSTAN "SALAVAT MEDICAL COLLEGE"

COURSE WORK

ACUTE CORONARY SYNDROME

Performed by Shavyrova Inna Sergeevna

Student of the specialty 31.02.01

Groups 401 F

WRC Manager

Artamonov Dmitry Viktorovich

salavat 2015

Introduction

Despite advances in the treatment of cardiovascular diseases, including the emergence of a large number of effective drugs, introduction into wide clinical practice of angioplasty and surgical techniques treatment, CVD continues to be the leading cause of morbidity and mortality in the world, claiming 17 million lives annually.

The first place in the structure of mortality from diseases of the circulatory system is ischemic disease hearts. In the materials of the WHO, it is characterized as an epidemic of the 21st century, being the main problem in the clinic of internal diseases. Annually in Russian Federation 166 000 cases of acute coronary syndrome are registered. The mortality rate reaches 39%, while the hospital mortality rate ranges from 12 to 15%.

About 50% die within the first 15 minutes;

IN last years the term "acute coronary syndrome" has become widespread. It includes acute variants of coronary artery disease: unstable angina pectoris, myocardial infarction (with and without elevation of the ST segment). Since unstable angina pectoris and myocardial infarction are indistinguishable in the clinic, at the first examination of the patient, after registering an ECG, one of two diagnoses is established.

Acute coronary syndrome serves as a preliminary diagnosis, allows the paramedic to determine the order and urgency of diagnostic and therapeutic measures. The main purpose of introducing this concept is the need to use active methods of treatment (thrombolytic therapy) until the final diagnosis is restored (presence or absence of large-focal myocardial infarction).

The final diagnosis of a specific variant of acute coronary syndrome is always retrospective. In the first case, the development of myocardial infarction with a Q wave is very likely, in the second, it is more likely: unstable angina pectoris or the development of myocardial infarction without a Q wave. The division of acute coronary syndrome into two options is primarily necessary for the early onset of targeted therapeutic measures: in acute coronary syndrome with elevation of the ST segment indicates the appointment of thrombolytics, and in acute coronary syndrome without ST elevation, thrombolytics are not indicated. It should be noted that in the process of examining patients, a "non-ischemic" diagnosis may be revealed, for example, PE, myocarditis, aortic dissection, neurocirculatory dystonia, or even extracardiac pathology, for example, acute diseases of the abdominal cavity.

Considering the complexity of pathogenesis, individual characteristics of the organism, as well as the changing contribution of each risk factor in the process of progression and development of acute coronary syndrome, the choice of a rational plan for prevention and differential diagnosis is challenging task... This circumstance makes it extremely difficult to predict the outcome of the disease and optimize the patient's treatment.

The relevance of this work is determined by the fact that the problem of ACS is one of the main causes of disability and death among the working population. There is an increase in lethal outcomes due to the number of deaths at the prehospital stage, in this regard, the role of a paramedic in the diagnosis and provision of first aid to patients with ACS is of particular importance.

Research objectives:

The relevance of this work is determined by the fact that the problem of ACS is one of the main causes of disability and death among the working population. There is an increase in deaths due to the number of deaths at the prehospital stage.

Of patients who die of myocardial infarction within the first 24 hours:

About 50% die within the first 15 minutes;

About 30% - within 15-60 minutes;

About 20% - within 1-24 hours.

Objective of the study: to identify the role of a paramedic at the prehospital stage in the management of patients with ACS.

Object of research: patients with ACS at the prehospital stage.

Research subject: ACS at the prehospital stage.

Research hypothesis:

Research objectives:

1. To study the tactics of managing patients with ACS at the prehospital stage according to literature data.

2. To identify cases of ACS in the emergency department of the city of Salavat in 2014.

3. Analyze the statistics of ACS in the emergency department of the city of Salavat, compare cases of unstable angina pectoris and myocardial infarction, determine the pattern of development of the syndrome by gender, age, seasonal and temporal characteristics.

4. Determine the role of a paramedic at the prehospital stage in the provision of emergency care in ACS.

Research methods. A comparative analysis of the statistical data on the number of patients with acute coronary syndrome attending the hospital in Salavat was carried out. 710 cases were identified. Statistical data processing was carried out on a personal computer using Microsoft Office software (Word, Excel).

1. Theory part

Acute coronary syndrome - a collective concept that includes conditions caused by acute progressive myocardial ischemia.

ACS without ST segment elevation:

Unstable angina pectoris:

1.First-onset angina pectoris;

2. Progressive exertional angina;

3. Spontaneous exertional angina;

4. Variant angina pectoris (Prinzmetal);

Myocardial infarction without ST segment elevation;

Differential diagnosis between these two conditions on the EMS is not carried out, therefore they are combined with the term "acute coronary syndrome without ST segment elevation"

ACS with ST segment elevation:

Myocardial infarction with the rise of the ST segment in the first hours of the disease and the subsequent formation of the Q wave, which is considered separately.

Etiology

Reasons for the development of ACS	Description of ACS development factors
Atherosclerosis of the coronary arteries (95 - 97%)	With complete thrombotic occlusion of the coronary artery, transmural MI (Q-wave MI) develops. When a parietal thrombus forms, a non-transmural MI (MI without a Q wave) is formed.
Severe and prolonged spasm of the coronary arteries	Can cause myocardial infarction in young and middle-aged people without arterial damage by atherosclerotic plaques.
For various diseases internal organs (being not a form of ischemic heart disease, but a complication of the main process)	With aortic heart defects - as a result of relative coronary insufficiency; When infective endocarditis - due to thromboembolism in the coronary arteries; With rheumatic fever and other pathologies connective tissue - due to inflammatory lesions of the coronary arteries; With disseminated intravascular coagulation and other blood diseases accompanied by blood coagulation disorders - as a result of thrombosis of unchanged coronary arteries.

Pathogenesis

In the pathogenesis of myocardial infarction, the leading role belongs to the cessation of blood flow to the area of \u200b\u200bthe heart muscle, which leads to damage to the myocardium, its necrosis, and deterioration of the vital activity of the peri-infarction zone.

Myocardial necrosis is manifested by resorption-necrotic syndrome (data laboratory research, increase in body temperature) is confirmed by ECG data. It causes long-term pain syndrome, can manifest itself by the development of arrhythmias and heart block, and transmural necrosis - by heart ruptures or acute aneurysms.

Myocardial necrosis, violation of the state of the peri-infarction zone contribute to a decrease in stroke and cardiac output. Clinically, this is manifested by the development of acute left ventricular failure - pulmonary edema and (or) cardiogenic shock. The latter is accompanied by a sharp decrease in the blood supply to vital organs, which leads to impaired microcirculation, tissue hypoxia and the accumulation of metabolic products.

Metabolic disorders in the myocardium are the cause of severe heart rhythm disturbances, often ending in ventricular fibrillation.

The decrease in coronary blood flow resulting from cardiogenic shock further contributes to a decrease in the pumping function of the heart and aggravates the course of cardiogenic shock and pulmonary edema - the main causes of death in MI.

Classification myocardial infarction

By the magnitude of necrosis:	Q wave MI (transmural, large-focal). MI without Q wave (small focal, subendocardial).
With the flow:	· Primary MI - in the absence of anamnestic and instrumental signs of previous MI. · Recurrent MI - when new areas of necrosis appear within 72 hours to 4 weeks after the development of MI (the appearance of new foci of necrosis in the first 72 hours of MI is not a relapse, but an expansion of the MI zone). · Recurrent myocardial infarction is not associated with primary myocardial necrosis and develops in the basin of other coronary arteries in periods exceeding 4 weeks from the onset of the previous MI. · MI with a protracted course (with a long period of pain attacks, slowed down reparation processes).
By localization:	MI of the anterior wall of the left ventricle: Anterior septal; Anterior apical; Anterolateral; High front; Widespread anterior. MI of the posterior wall of the left ventricle: Posterior diaphragmatic or inferior; Posterior basal; Widespread posterior. MI of the right ventricle (very rare).
By periods:	· The most acute - from 30 minutes to 2 hours from the beginning of myocardial infarction. · Acute - up to 10 days from the onset of MI. · Subacute - from the 10th day of myocardial infarction until the end of 4-8 weeks. Postinfarction - after 4-8 weeks of MI up to 2-6 months.
Clinical options for the onset of myocardial infarction:	Painful or anginal (status anginosus); Asthmatic (status asthmaticus); Abdominal or gastralgic (status abdominalis); · Arrhythmic; · Cerebral; · Painless (low-symptom); · With atypical localization of pain.

2. Clinical picture

ACS clinic at the prehospital stage is manifested by the most acute period of myocardial infarction (the time between the onset of the first symptoms of acute myocardial ischemia and the appearance of signs of its necrosis). In this period, the morphological changes in the heart muscle are still reversible, and with timely thrombolysis, the restoration of coronary blood flow is possible.

Clinical variants of acute myocardial infarction.

	Anginal pain, independent of posture and position body, from movement and breathing, resistant to nitrates. The pain has a pressing, choking, burning or tearing character with localization behind the sternum, in the entire anterior chest wall with possible irradiation to the shoulders, neck, arms, back, epigastric region. It is characterized by a combination with hyperhidrosis, severe general weakness, pallor of the skin, agitation, motor restlessness.
Abdominal	Combination of epigastric pain with dyspeptic symptoms: nausea, which does not bring relief from vomiting, hiccups, belching, abdominal distension; possible irradiation of back pain, tension of the abdominal wall and pain on palpation in the epigastrium
Atypical painful	Pain syndrome - has atypical localization (for example, only in areas of irradiation: throat and lower jaw, shoulders, arms, etc.)
Asthmatic	Shortness of breath (feeling short of breath - equivalent to angina), which is a manifestation of acute heart failure (cardiac asthma or pulmonary edema)
Arrhythmic	Rhythm disturbances prevail

Characteristics of pain in a typical variant of myocardial infarction:

Atypical forms of acute coronary syndrome:

3. Complications

Heart rhythm and conduction disorders.

Acute heart failure.

Cardiogenic shock.

Mechanical complications: ruptures (interventricular septum,

free wall of the left ventricle), detachment of the mitral valve chords,

separation or dysfunction of the papillary muscles).

Pericarditis (episthenocarditis and with Dressler's syndrome).

Prolonged or recurrent pain attack, postinfarction angina.

4. Diagnostics and advice of a paramedic

First of all, other causes of pain should be excluded.

ma, requiring immediate assistance and hospitalization:

Acute aortic dissection

Ruptured esophagus

Acute myocarditis

Bleeding from the upper gastrointestinal tract.

Before the arrival of the ambulance brigade:

1. Lay the patient down with a slightly raised head end.

2. Absolute bed rest.

3. Provide warmth and rest.

4. Give the patient nitroglycerin under the tongue (1-2 tablets or spray 1-2 doses), if necessary, repeat the dose after 5 minutes.

5. If the painful attack lasts more than 15 minutes, give the patient 160-325 mg to chew acetylsalicylic acid.

6. Find the drugs that the patient is taking, the ECG taken earlier, and show them to the EMS staff.

7. Do not leave the patient unattended.

When did the attack of chest pain start? How long does it take?

What is the nature of the pain? Where is it localized and is there any irradiation?

Have there been attempts to stop the attack with nitroglycerin?

Does the pain depend on posture, body position, movement and breathing? (no myocardial ischemia)

What are the conditions for the onset of pain (exercise, excitement, cooling, etc.)?

Did the attacks (pain or choking) occur during exercise (walking), did they make you stop, how long did they last (in minutes), how did they react to nitroglycerin? (The presence of exertional angina makes the assumption of acute coronary syndrome highly probable)

Does a real attack resemble the sensations that arose during physical exertion in terms of the location or nature of the pain?

Frequent, have the pain intensified recently? Has your exercise tolerance changed or your nitrate requirement has increased?

Are there risk factors for cardiovascular disease: smoking, arterial hypertension, diabetes mellitus, hypercholesterol, or triglyceridemia? (Risk factors are of little help in diagnosing myocardial infarction, but they increase the risk of complications and / or death)

Assessment of the general condition and vital functions: consciousness, respiration, blood circulation.

Visual assessment: skin pale, high humidity, specify the presence of swelling of the cervical veins - a prognostically unfavorable symptom.

Pulse study, heart rate calculation (tachycardia, bradycardia).

Calculation of NPV: increasing shortness of breath is a prognostically unfavorable symptom.

Measurement of blood pressure in both arms: hypotension is a prognostically unfavorable symptom.

Percussion: the presence of an increase in the boundaries of relative cardiac dullness (cardiomegaly).

Palpation (does not change the intensity of pain): assessment of the apical impulse, its localization.

Auscultation of the heart and blood vessels (assessment of tones, presence of murmurs):

The presence of a III heart sound or the presence of an IV heart sound;

The appearance of a new murmur in the heart or an increase in the previous one.

Auscultation of the lungs: wet wheezing is a prognostically unfavorable symptom.

It should be borne in mind that in many cases the physical examination does not reveal abnormalities.

coronary ischemic infarction angina pectoris

5. Instrumental research

ECG diagnostics.ECG - signs of ACS

	arcuate segment rise STconvex upward, merging with a positive tooth .
	arcuate segment rise STbulge upward, passing into a negative tooth T.
	arcuate segment depression STbulging down, merging with a positive tooth T.
	the appearance of a pathological tooth Qand a decrease in the amplitude of the wave R.
	tooth disappearance Rand the formation QS.
	negative symmetrical wave T.

Laboratory diagnostics.

In acute coronary syndrome, a study of the level of biomarkers of myocardial infarction (troponin, MB-creatine phosphokinase, myoglobin) is carried out. In the conditions of the EMS, it is possible to use kits for express diagnostics of increased troponin levels in the blood.

ECG signs of acute myocardial infarction (in the absence of LVH and LBBB):

Localization of myocardial infarction by pathological signs on the ECG:

Localization of IM	ECG leads with signs of MI
Anterior septal MI	I, aVL, V 1 - V 3
Anterior apical
Anterolateral	I, aVL. V 5 - V 6
High side
Widespread anterior	I, aVL, V 1 -V 6. In the Sky - Anterior (A)
Posterior diaphragmatic (lower)	III, II, aVF, in the sky - Inferior (I)
Posterior basal	V 7 - V 9, in the sky - Dorsalis (D)
Widespread posterior	II, III, aVF, V 5 - V 9 in the Sky - I and D

Troponin - a contractile protein of cardiomyocytes, is not normally detected in the blood. A positive test result for the troponin level by the express method confirms myocardial infarction, but it should be remembered that the level of troponin can increase in other conditions (for example, PE).

A negative result does not exclude this diagnosis, because troponin is recorded in the blood only a few hours after the onset of ischemia. Therefore, the troponin test should be repeated after 6-8 hours in the hospital, and if its level is again normal, then unstable angina pectoris occurs.

6. Treatment

The patient's position: lying on his back with his head slightly raised.

Nitroglycerin under the tongue in tablets (0.5-1 mg), aerosol or spray (0.4-0.8 mg or 1-2 doses) for unloading the heart and relieving pain. If necessary and normal blood pressure, repeat every 5-10 minutes.

The combination of Acetylsalicylic acid and Clopidogrel is indicated for all patients. Acetylsalicylic acid (if the patient did not take it on his own before the arrival of the EMS) chew 250 mg. The drug is quickly and completely absorbed, after 30 minutes it reaches its maximum effect, inhibits platelet aggregation and has an analgesic effect, reduces mortality in myocardial infarction. Contraindications: hypersensitivity, erosive and ulcerative lesions of the gastrointestinal tract in the acute stage, gastrointestinal bleeding, aortic dissection, hemorrhagic diathesis, "aspirin" asthma, portal hypertension, pregnancy (I and III trimesters). Clopidogrel (Plavix) 300 mg in a loading dose.

Oxygen therapy - inhalation of humidified oxygen is carried out using a mask or through a nasal catheter at a rate of 3-5 l / min.

To relieve pain, the use of narcotic analgesics is indicated.

Dilute morphine 1 ml of a 1% solution in 20 ml of 0.9% sodium chloride solution (1 ml of the resulting solution contains 0.5 mg of the active substance) and inject intravenously in divided doses of 4-10 ml (or 2-5 mg) every 5 -15 minutes until pain and shortness of breath are eliminated or until side effects appear (hypotension, respiratory depression, vomiting). Total dose<20 мг. При побочных эффектах морфина (гипотония и брадикардия) - вводят Атропина сульфат 0,1% раствора 0,5-1,0 мг внутривенно, при угнетении дыхания -Налоксона гидрохлорид (0,04% раствор) 0,4мг/1млвнутривенно медленно за 3-5 минут, при необходимости повторно через 15 минут эту же дозу, при тошноте и рвоте - Метоклопрамид (0,5% раствор - 2-4 мл) 10-20 мг внутримышечно или внутривенно.

Nitroglycerin - 10 ml of a 0.1% solution is diluted in 100 ml of 0.9% sodium chloride solution (concentration 100 mg / ml) and injected intravenously under constant control of blood pressure and heart rate. When using an automatic dispenser, the initial injection rate is 5-10 μg / min; in the absence of a dispenser, the initial rate is 2-4 drops per minute, which can be gradually increased to a maximum rate of 30 drops per minute (or 3 ml / min). Stop infusion when SBP decreases<90 мм рт.ст. (или среднего АД на 20% от исходного), так как это снижение приводит к ухудшению коронарной перфузии и к увеличению зоны инфаркта миокарда, а также при возникновении выраженной головной боли. Следует помнить, что раствор быстро разрушается на свету, поэтому флаконы и систему для переливания необходимо закрывать светонепроницаемым материалом.

Segment elevation myocardial infarctionST in two or more leads or with a blockade of the left bundle branch

Segment lifting STindicates an acute occlusion of the coronary artery and myocardial ischemia, therefore, restoration of blood flow due to the dissolution of a thrombus (thrombolysis) prevents or reduces necrosis of the area of \u200b\u200bthe heart muscle that has lost blood supply.

If the total time from the onset of pain in the heart to the patient's transportation to the hospital can exceed 60 minutes, then the issue of prehospital use of thrombolytics should be resolved.

Thrombolysis method:

Thrombolytic drugs are administered only through peripheral veins; attempts to catheterize the central veins are unacceptable; exclude i / m injection.

Streptokinase - 1.5 million IU is injected intravenously for 30-60 minutes. Sodium heparin is not administered, acetylsalicylic acid is sufficient.

Alteplase - 15 mg IV bolus, then 0.75 mg / kg (maximum 50 mg) for 30 min, then 0.5 mg / kg (maximum 35 mg) for 60 minutes. It is necessary in addition to acetylsalicylic acid in / in bolus to inject sodium heparin 60 mg / kg (maximum 4000 IU). The efficiency of alteplase is comparable to that of streptokinase. The use of alteplase is advisable in patients who have used streptokinase in the past.

The effectiveness of thrombolytic therapy is assessed by segment reduction STby 50% of the initial elevation within 1.5 hours and the appearance of reperfusion rhythm disturbances (accelerated idioventricular rhythm, ventricular extrasystole, etc.)

Complications of thrombolytic therapy:

Arterial hypotension during infusion - raise the patient's legs, reduce the infusion rate.

Allergic reaction (usually to streptokinase) - prednisolone 90-150 mg IV bolus, with anaphylactic shock - epinephrine 0.5-1 ml of 0.1% solution in / m.

Bleeding from puncture sites - press the puncture site for 10 minutes. Uncontrolled bleeding - stop the introduction of thrombolytics, transfusion of fluids, it is permissible to use aminocaproic acid 100 ml of a 5% solution IV drip for 60 minutes. Recurrence of pain syndrome - nitroglycerin IV drip.

Reperfusion arrhythmias - treatment as for rhythm and conduction disturbances of other etiology - if necessary, cardiopulmonary resuscitation, cardioversion, etc.

Stroke. Algorithm for making a decision on thrombolysis:

Acute coronary syndrome without segment elevationST or myocardial infarction with segment elevationST if thrombolytic therapy is impossible

In order to prevent the spread of an existing thrombus and the formation of new ones, anticoagulants are used. Remember that anticoagulants are contraindicated against the background of a hypertensive crisis.

Heparin sodium - i.v. bolus of 60 IU / kg (4000-5000 IU). The action develops a few minutes after intravenous administration, lasts 4-5 hours. Possible side effects: allergic reactions, a feeling of heat in the soles, pain and cyanosis of the extremities, thrombocytopenia, bleeding and bleeding. Contraindications: hypersensitivity, bleeding, erosive and ulcerative lesions of the gastrointestinal tract, severe arterial hypertension, diseases manifested by increased bleeding (hemophilia, thrombocytopenia, etc.), esophageal varices, chronic renal failure, recent surgical interventions on the eyes, brain, prostate gland, liver and biliary tract, condition after spinal cord puncture. It is used with caution in persons suffering from polyvalent allergies and during pregnancy.

Low molecular weight heparins, which have anticoagulant and antithrombotic effects, have a lower incidence of severe side effects, and are convenient to use, are recognized as a viable alternative to unfractionated heparin.

Nadroparin calcium (fraxiparin) - s / c, dose 100 IU / kg (which corresponds to 0.4-0.5 ml at 45-55 kg; 55-70 kg - 0.5-0.6 ml; 70- 80 kg - 0.6- 0.7 ml; 80-100 kg - 0.8 ml; over 100 kg - 0.9 ml). During the injection of the contents of a single-dose syringe into the subcutaneous tissue of the abdomen, the patient should lie down. The needle is inserted vertically along its entire length into the thickness of the skin, squeezed into the fold between the thumb and forefinger. The skin fold is not straightened until the end of the injection. Do not rub the injection site after injection. Contraindications - see above "Heparin sodium".

To reduce myocardial oxygen demand, to reduce the area of \u200b\u200bmyocardial infarction, the use of b-blockers is shown. The appointment of b-blockers in the first hours and their subsequent long-term use reduces the risk of death.

Propranolol (non-selective b-blocker) - intravenous stream, slowly inject 0.5-1 mg, it is possible to repeat the same dose after 3-5 minutes until a heart rate of 60 per minute is reached under the control of blood pressure and ECG. Contraindicated in arterial hypotension (SBP<100 мм рт.ст.), брадикардии (ЧСС <60 в минуту), острой сердечной недостаточности (отёк лёгких), облитерирующих заболеваниях артерий, бронхиальной астме, беременности. Допустим пероральный приём 20 мг.

If there are complications, they are treated.

Cardiogenic shock: vasopressors (catecholamines).

Pulmonary edema: give the patient an elevated position, dehydration - diuretics, as indicated by vasopressors.

Heart rhythm and conduction disorders: with unstable hemodynamics - cardioversion; for ventricular arrhythmias, the drug of choice is amiodarone; with bradyarrhythmia - Atropine sulfate 0.1% solution of 0.5-1.0 mg intravenously.

Vomiting and nausea: Metoclopramide (0.5% solution - 2-4 ml) 10-20 mg intramuscularly or intravenously.

Indications for hospitalization

Myocardial infarction or acute coronary syndrome is a strong indication for hospitalization in the intensive care unit or cardiac intensive care unit. The slightest suspicion of ischemic genesis of chest pain, even in the absence of characteristic electrocardiographic changes, should be a reason for the immediate transportation of the patient to the hospital. Transportation is carried out lying on a stretcher with a slightly raised head end.

Common application errors

Three-step scheme of pain relief: if sublingual nitroglycerin is ineffective, narcotic analgesics are switched to narcotic analgesics only after an unsuccessful attempt to relieve pain syndrome using a combination of a non-narcotic analgesic (analgin © [INN: sodium metamizole]) with an antihistamine (diphenhydramine: diphenyl) [MHNH

The introduction of drugs in / m, because it makes it impossible to subsequently carry out fibrinolysis and contributes to false results of the study of the level of creatine phosphokinase.

The use of myotropic antispasmodics.

The use of atropine for the prevention of vagomimetic effects of morphine.

Prophylactic administration of lidocaine.

The use of dipyridamole, potassium and magnesium aspartate.

Methods of application and dosage of drugs at the EMP stage application

Nitroglycerin (for example, nitrocor), tablets of 0.5 and 1 mg; aerosol of 0.4 mg in 1 dose.

Adults: sublingual 0.5-1 mg tablets or sublingual inhalation 0.4-0.8 mg (1-2 doses). Repeat if necessary after 5 minutes.

Nitroglycerin (nitroglycerin), 0.1% solution in 10 ml ampoules (1 mg / ml).

Adults: intravenous drip - 10 ml of 0.1% solution is diluted in 100 ml of 0.9% sodium chloride solution, the rate of administration is 5-10 mcg / min (2-4 drops per minute) under constant blood pressure control and heart rate. The infusion rate can be gradually increased to a maximum of 30 drops per minute (or 3-4 ml / min).

Acetylsalicylic acid (aspirin) tablets of 50, 100, 300 and 500 mg.

Adults: 100-300 mg per day.

Propranolol (for example, anaprilin, obzidan) 0.1% solution in 5 ml ampoules (1 mg / ml).

Adults: 0.5-1 mg (0.5-1 ml) is slowly injected intravenously.

Morphine (morphine hydrochloride) 1% solution in 1 ml ampoules (10 mg / ml).

Adults: dilute 1 ml in 20 ml of 0.9% sodium chloride solution and inject intravenously in fractional amounts of 4-10 ml every 5-15 minutes until pain and shortness of breath are eliminated, or until side effects (arterial hypotension, depression) appear. breathing, vomiting).

Streptokinase (streptase), lyophilisate for the preparation of a solution for infusion in vials of 1.5 million IU.

Adults: 1.5 million IU is injected IV over 60 minutes.

Alteplase (Aktilize) is a lyophilisate for the preparation of a solution for infusion in 50 mg vials.

Adults: 15 mg IV bolus followed by 0.75 mg / kg (maximum 50 mg) over 30 minutes, then 0.5 mg / kg (maximum 35 mg) over 60 minutes.

Sodium heparin (for example, heparin) 5 thousand IU / ml in 5 ml ampoules. Nadroparin calcium (fraxiparin) 9.5 thousand IU (anti-Xa) / ml, single-dose syringes, 0.3 each; 0.4; 0.6; 0.8 and 1.0 ml.

45-55 kg - 0.4-0.5 ml;

55-70 kg - 0.5-0.6 ml;

70-80 kg - 0.6- 0.7 ml;

80-100 kg - 0.8 ml;

More than 100 kg - 0.9 ml.

Analysis of the number of ACS cases in the emergency department for the period 2012-2014:

Fig. 1. Quantitative analysis of ACS cases in the emergency department for the period 2012-2014

During the study period, 1367 cases of ACS were identified. Of these, 36% are cases of 2014, 33% - 2013, 31% are in 2012.

Fig. 2. Quantitative analysis of cases of MI and NA

Analysis of MI and NS cases:

Among ACS in 2014, MI accounted for 32% of cases, NS - 68%; for 2013 IM - 29%, NS - 71, 2014 IM - 28%, NS - 72%.

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MULTICENTER RESEARCH OF CHEST PAIN% Stabbing pain in the chest Pain with lesions of the pleura Pain on palpation ACUTE MYOCARDIAL ISCHEMIA WAS DETECTED AT…. Lee T., Cook E., et al. 1985

DOCTOR'S TACTICS FOR ACS IN THE PREHOSITIONAL STAGE Initial assessment of patients with chest pain. Differential diagnosis. Indication for hospitalization and transportation. Pre-hospital assessment of the risk of death and development of AMI in patients with ACS without ST-segment elevation.

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DOCTOR'S TACTICS IN ACS AT THE PREHOSPITAL STAGE Initial assessment of patients with chest pain. Differential diagnosis. Indication for hospitalization and transportation. Prehospital assessment of the risk of death and MI in patients with ACS. Treatment of CSCs at the prehospital stage.

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12.5 6.4 5.3 2.0 Influence of aspirin and heparin on the sum of deaths and myocardial infarction in ACS without ST Meta-analysis of the conducted studies p \u003d 0.0005 Aspirin 5 days-2 years Heparin 1 week No treatment% n \u003d 2488 n \u003d 2629

Factors influencing the choice of antithrombotic treatment for ACS without persistent ST The nature of myocardial ischemia and time after the last episode Risk of adverse outcome (MI, death) in the near future Approach to patient management invasive conservative Clinical judgment on the presence of ongoing intracoronary thrombosis Risk of bleeding Renal function

Initial Dose Long-term use Class European Society of Cardiology, ACS without ST (2002) with clopidogrel I (A) I (A) American College of Cardiology and Heart Association, ACS without ST (2002) I (A) I (A) Russian recommendations, ACS without ST (2004), then (150) - European Society of Cardiology, antiplatelet agents (2004) I (A) I (A) American College of Thoracic Physicians (2004) I (A) I ( A) Eur Heart J 2002; 23: Circulation 2002; 106: Chest 2004; 126: 513S-548S. Eur Heart J 2004; 25: Cardiology 2004, supplement. Aspirin for ACS without ST. Modern guidelines

Heparin in ACS without persistent ST on ECG for pain IV infusion of UFH SC injections of LMWH High risk of thrombotic complications ST troponin ... No signs of high risk of thrombotic complications no ST normal troponin (twice with an interval of\u003e 6 hours) Observation 6-12 hours Introduction from 2 to 8 days (according to the doctor's decision) Cancellation of heparin 6 hours "\u003e 6 hours) Observation 6-12 hours Introduction from 2 to 8 days (by the doctor's decision) Cancellation of heparin"\u003e 6 hours "title \u003d" (! LANG: Heparin for ACS without persistent ST on ECG 48-72 hours from pain I / V infusion of UFH SC injections of LMWH High risk of thrombotic complications ST troponin ... No evidence of high risk of thrombotic complications No ST normal troponin (twice with an interval of\u003e 6 h"> title="Heparin in ACS without persistent ST on ECG 48-72 h of pain IV infusion of UFH SC injections of LMWH High risk of thrombotic complications ST troponin ... No evidence of high risk of thrombotic complications no ST normal troponin (twice with an interval of\u003e 6 h"> !}

Circulation 2003; 107: 966–72 0.00 0.02 0.04 0.06 0.08 0.10 0.12 0, Months 9.3% 11.4% C-s death, MI, stroke, severe ischemia Aspirin Hours after randomization Aspirin + clopidogrel risk 34% p \u003d 0.003 Risk of event Heparin in 92%, of which LMWH 54% Clopidogrel addition in ACS without ST CURE study (n \u003d 12 562)

Clopidogrel in addition to aspirin for non-ST ACS Current guidelines Duration Class European Society of Cardiology (2002) minimum 9 months possibly 12 months I (B) I (B) American College of Cardiology and Heart Association (2002) minimum 1 month to 9 month I (A) I (B) I (A) I (B) Russian guidelines (2004) about 1 year - American College of Thoracic Physicians (2004) 9-12 months I (A) I (A) European Cardiology society, PCI (2005) 9-12 months I (B) I (B) Clopidogrel (loading dose 300 mg, then 75 mg / day) as early as possible Eur Heart J 2002; 23: Circulation 2002; 106: Chest 2004; 126: 513S-548S. Cardiology 2004, supplement. Eur Heart J 2005; 26:

Clinical variants of MI% status anginosus status asthmaticus status gastralgicus arrhythmic cerebral asymptomatic, 6 10.5 6.7 14.3 - 2.9 616 people 105 people A.L. Syrkin.

The clinical picture of ACS; - the appearance of pathological Q waves on the ECG; - ECG changes, indicating the appearance of myocardial ischemia: the occurrence of elevation or depression of the ST segment, blockade of LPH; Necessary and sufficient signs for the diagnosis of AMI One of the following criteria is sufficient for the diagnosis of AMI:

50% of deaths from STEMI occur in the first 1.5-2 hours from the onset of an anginal attack, and most of these patients die before the arrival of the emergency medical team. Therefore, the greatest efforts should be made so that first aid is provided to the patient as early as possible, and so that the volume of this aid is optimal.

A two-stage system, when, upon suspicion of MI, the linear ambulance team calls upon itself a "specialized" one, which actually begins treatment and transports the patient to the hospital, leads to an unjustified loss of time. Each ambulance team (including the paramedic) must be ready for active treatment STEMI patient Organization of EMS work in AMI Treatment of a STEMI patient is a single process that begins at the prehospital stage and continues in the hospital. For this, the ambulance teams and hospitals where ACS patients are admitted must work according to a single algorithm based on common principles of diagnosis, treatment and a common understanding of tactical issues.

Any ambulance team, having diagnosed ACS, having determined the indications and contraindications for appropriate treatment, should stop the pain attack, begin antithrombotic treatment, including the administration of thrombolytics (if invasive restoration of coronary artery patency is not planned), and with the development of complications - cardiac arrhythmias or acute cardiac insufficiency - the necessary therapy, including measures for cardiopulmonary resuscitation, Emergency care teams in each locality should have clear instructions to which hospitals to transport patients with STEMI or suspected STEMI Doctors of these hospitals, if necessary, provide emergency medical services with appropriate advice.

1. Portable ECG with autonomous power supply; 2. Portable device for EIT with autonomous power supply with heart rate control; 3. Set for cardiopulmonary resuscitation, including a device for manual ventilation; 4. Equipment for infusion therapy, including infusomats and perfusers; 5. Set for the installation of an IV catheter; 6. Cardioscope; 7. Pacemaker; 8. System for remote ECG transmission; 9. Mobile communication system; 10. Suction; 11. Medicines required for basic therapy of AMI The linear EMS team must be equipped with the necessary equipment

Each ambulance team (including the paramedic) should be ready for active treatment of the patient with STEMI Treatment of uncomplicated STEMI at the prehospital stage Basic therapy. 1. Eliminate pain syndrome. 2. Chew a tablet containing 250 mg ASA. 3. Take 300 mg of clopidogrel by mouth. 4. Start IV infusion of NG, primarily with persisting angina pectoris, AH, AHF. 5. Start treatment with b-blockers. Preferably the initial intravenous administration, especially with ischemia, which persists after intravenous administration of narcotic analgesics or recurs, hypertension, tachycardia or tachyarrhythmia, without HF. It is planned to perform primary TBA. Loading dose of clopidogrel mg.

90 If ineffective, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 minutes or 4-8 mg + 2 mg every "title \u003d" (! LANG : Providing emergency care Anesthesia Nitroglycerin 0.4 mg p / i or spray for systolic blood pressure\u003e 90 If ineffective, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5- 15 min or 4-8 mg + 2 mg every" class="link_thumb"> 38 !} Providing emergency care Anesthesia Nitroglycerin 0.4 mg p / i or spray for systolic blood pressure\u003e 90 If ineffective, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg mg every 5-15 minutes or 4- 8 mg + 2 mg every 5 minutes or 3-5 mg until pain relief IV nitroglycerin with blood pressure\u003e 90 mm Hg, if there is pain, acute pulmonary congestion, high blood pressure Nitroglycerin 0.4 mg p / i or spray with SBP\u003e 90 With ineffectiveness "03" 90 If ineffective, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 minutes or 4-8 mg + 2 mg every "\u003e 90 If ineffective, after 5 min Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 minutes or 4-8 mg + 2 mg every 5 minutes or 3-5 mg until pain relief B \\ into nitroglycerin with blood pressure\u003e 90 mm Hg, if there is pain, acute congestion in the lungs, high blood pressure Nitroglycerin 0.4 mg p / i or spray with systolic blood pressure\u003e 90 With ineffectiveness "03" "\u003e 90 With ineffectiveness, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 minutes or 4-8 mg + 2 mg every "title \u003d" (! LANG: Emergency care Pain relief Nitroglycerin 0, 4 mg p / i or spray for systolic blood pressure\u003e 90 If ineffective, after 5 minutes Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 minutes or 4-8 mg + 2 mg every"> title="Emergency care Anesthesia Nitroglycerin 0.4 mg p / i or spray for systolic blood pressure\u003e 90 If ineffective, after 5 min Morphine (especially with agitation, acute heart failure) IV 2-4 mg + 2-8 mg every 5-15 min or 4-8 mg + 2 mg every"> !}

Possible complications when using morphine Severe hypotension. A horizontal position in combination with raising the legs (if there is no pulmonary edema). If ineffective, IV - 0.9% NaCl solution or other plasma expanders. In rare cases, pressor drugs. Severe bradycardia in combination with hypotension; eliminated by atropine (intravenously 0.5-1.0 mg). Nausea, vomiting; eliminated by phenothiazine derivatives, in particular, metoclopramide (intravenously 5-10 mg). Severe respiratory depression; eliminated by naloxone (intravenously 0.1-0.2 mg, if necessary again after 15 minutes), however, the analgesic effect of the drug also decreases.

Nitrates in acute myocardial infarction Indications for the use of nitrates myocardial ischemia acute pulmonary congestion the need to control blood pressure p / i (spray) 0.4 mg up to 3 times every 5 minutes i.v. infusion (5-200 μg / min, average BP by 10% in normotonics, up to 30% with hypertension) inside while maintaining ischemia SBP 30 mm Hg below the baseline heart rate 100 suspected right ventricular infarction

Lancet 1995; 345: Nitrates in early dates MI Meta-analysis (n \u003d 81 908) 9 small, inside 11 small, i.v. GISSI-3 ISIS-4 All studies Nitrate Risk control 5.5% p \u003d 0.03

Prehospital triple antiplatelet therapy On-TIME 2 trial data Prehospital IH IIb / IIIa tirofiban (25 μg / kg bolus followed by 0.15 μg / kg / min infusion for 18 hours) or placebo in addition to aspirin (500 mg intravenously), clopidogrel (600 mg orally) and intravenous bolus (5000 IU) UFH p \u003d 0.043 p \u003d 0.051 p \u003d 0.581

Restoration of coronary perfusion The mainstay of treatment for acute MI is restoration of coronary blood flow - coronary reperfusion. The destruction of the thrombus and the restoration of myocardial perfusion lead to a limitation of the extent of its damage and, ultimately, to an improvement in the short and long term prognosis. Therefore, all STEMI patients should be promptly evaluated to clarify the indications and contraindications for the restoration of coronary blood flow. Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST segment elevation ECG, VNOK

Efficiency of TLT in MI, depending on the time of initiation of treatment 65 * Lives saved per 1000 treated 37 * 29 * 18 * 0-1 h 1-2 h 2-3 h 3-6 h Lancet 1996; 348: Death in the first 35 days 26 * h Time from the onset of symptoms to the introduction of a fibrinolytic n \u003d * p

Onset of pain Decision to call an ambulance Ambulance arrival Arrival to the hospital Clearance in the emergency room Diagnosis SK PTCA Metallize at the prehospital stage Prehospital thrombolysis: gain in time \u003d saving myocardium Actilize Metallize in the emergency room "Early thrombolysis" strategy Call for pain in the ICU tomorrow ambulance Arrival of ambulance Diagnosis

USIC 2000: Reducing Mortality in Prehospital Thrombolysis Danchin et al. Circulation 2004; 110: 1909 - Mortality (%) Dogosp. TLTL in hospital PCI Without reperfusion therapy

Choice of strategy WEST survey, n \u003d 304% EHJ, 2006; 27,

VIENNA STEMI REGISTRY: Change in reperfusion strategy VIENNA 2003/2004 VIENNA 2002 Kalla et al. Circulation 2006; 113: 2398 - Patients (%) PCI Without reperfusion Thrombolysis

Kalla et al. Circulation 2006; 113: 2398-2405. VIENNA STEMI REGISTRY: Time from disease onset to treatment with different THROMBOLYSIS PCI strategies 0-2 h 2-6 h Patients (%) 6-12 h

Years Eagle et al. 2007, Submitted GRACE REGISTRY Reperfusion therapy No reperfusion PCI only TLT only Patients (%)

Prehospital treatment of uncomplicated STEMI Prehospital thrombolytic therapy. It is carried out in the presence of indications and the absence of contraindications. When using streptokinase, at the discretion of the physician, direct-acting anticoagulants can be used as concomitant therapy. If anticoagulant use is preferred, UFH, enoxaparin, or fondaparinux may be chosen. When using fibrin-specific thrombolytics, enoxaparin or UFH should be used. Reperfusion therapy is not expected. The decision on the advisability of using direct anticoagulants may be postponed until admission to the hospital. Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST segment elevation ECG, VNOK

Indications for TLT If the time from the onset of an anginal attack does not exceed 12 hours, and the ECG shows an increase in the ST segment of 0.1 mV, at least in 2 consecutive chest leads or in 2 leads from the extremities, or there is a blockade of LDBH. The introduction of thrombolytics is justified at the same time with ECG signs of true posterior MI (high R waves in the right precordial leads and depression of the ST segment in leads V1-V4 with an upward T wave). Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST segment elevation ECG, VNOK

Contraindications for TLT. Absolute contraindications for TLT. Previous hemorrhagic stroke or CMC of unknown etiology; ischemic stroke, suffered during the last 3 months; brain tumor, primary and metastatic; suspicion of aortic dissection; the presence of signs of bleeding or hemorrhagic diathesis (with the exception of menstruation); significant closed head injuries in the last 3 months; changes in the structure of cerebral vessels, for example, arteriovenous malformation, arterial aneurysms Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST segment elevation ECG, VNOK

Checklist for making a decision by the medical and paramedic team of the ambulance service to conduct a patient with acute coronary syndrome (ACS) TLT Check and mark each of the indicators given in the table. If all the boxes in the "Yes" column are marked and none in the "No" column, then thrombolytic therapy is indicated to the patient. If there is even one unmarked box in the “Yes” column, TLT therapy should not be performed and the checklist can be stopped. "Yes" "No" The patient is oriented, can communicate Pain syndrome characteristic of ACS and / or its equivalents lasting at least min., But not more than 12 hours After the disappearance of pain syndrome characteristic of ACS and / or its equivalents, no more than 3 hours have passed. high-quality ECG registration in 12 leads The doctor / paramedic of the EMS has experience in assessing ST segment changes and bundle branch blockade on an ECG (test only in the absence of a remote ECG evaluation by a specialist) There is a ST segment elevation by 1 mm or more in two or more adjacent ECG leads or a blockade of the left bundle branch was registered, which the patient did not have before The doctor / paramedic of the emergency medical service has experience in performing TLT. Transportation of the patient to the hospital will take more than 30 minutes. It is possible to receive medical recommendations from a cardioreanimatologist of the hospital in real time. ECG monitoring (at least one lead), intravenous infusion th (a catheter is installed in the cubital vein) and urgent use of a defibrillator

CONCLUSION: TLT to the patient _____________________________ (full name) SHOWN CONTRAINDICATED (circle the necessary, cross out the unnecessary) The sheet was filled out by: Doctor / paramedic (circle the necessary) _________________________ (full name) Date ____________ Time _________ Signature _____________ The checklist is transferred with the patient to the hospital history and is filed 35 years for men and over 40 for women Systolic blood pressure does not exceed 180 mm Hg. Art. Diastolic blood pressure does not exceed 110 mm Hg. Art. The difference in systolic blood pressure levels measured on the right and left hand does not exceed 15 mm Hg. Art. There is no history of stroke or the presence of other organic (structural) brain pathology.There are no clinical signs of bleeding of any localization (including gastrointestinal and urogenital) or manifestations of hemorrhagic syndrome. The submitted medical documents do not contain data on the patient's long-term (more than 10 minutes) ) cardiopulmonary resuscitation or the presence of internal bleeding in the last 2 weeks; the patient and his relatives confirm this. In the submitted medical documents there is no data on the transferred over the last 3 months. surgery (including on the eyes using a laser) or serious injury with hematomas and / or bleeding, the patient confirms this The submitted medical documents do not contain data on the presence of pregnancy or the terminal stage of any disease and the survey and examination data confirm this The submitted medical documents do not contain data on the presence of jaundice, hepatitis, renal failure in the patient, and the data from the survey and examination of the patient confirm this.

Thrombolytic drugs Alleplaza Intravenous 1 mg / kg body weight (but not more than 100 mg): bolus 15 mg; subsequent infusion of 0.75 mg / kg of body weight in 30 minutes (but not more than 50 mg), then 0.5 mg / kg (but not more than 35 mg) in 60 minutes (total duration of infusion 1.5 hours). Purolaza Intravenous: bolus of ME followed by infusion of ME for min. Streptokinase By intravenous infusion (IU per minute). Tenecteplase Intravenous bolus: 30 mg at a weight of 90 kg. Russian recommendations. Diagnostics and treatment of patients with acute myocardial infarction with ST segment elevation ECG, VNOK

Evolution of thrombolysis First generation Second generation Third generation Streptokinase allergenic not selective to fibrin Continuous intravenous infusion Actilise "gold standard" fibrin selectivity not allergenic Metalysis Equivalent to Alteplase High fibrin specificity Single bolus 5-10 seconds

Meta-analysis of studies with early intravenous administration of beta-blockers in MI (n \u003d 52 411) Lancet 2005; 366:% -22% -15% Death Recurrent MI VF and other causes of cardiac arrest

IV% 50% BETA-BLOCKERS: APPLICATION IN PATIENTS WITH ACS IN 59 RUSSIAN CENTERS GRACE register data (years) N \u200b\u200b\u003d 2806 C ST –50.3% Without ST - 49.7% C ST Without ST 0% IV 4.3% 100 % 50% 0% Previous 7 days First 24 hours. During the period of hospitalization Recommended. at discharge

Beta-blockers in STEMI Drug Dose Treatment on the 1st day of the disease Metoprolol IV 5 mg 2-3 times with an interval of at least 2 min; First oral administration 15 minutes after intravenous administration. Propronolol V / in 0.1 mg / kg for 2-3 doses at intervals of at least 2-3 minutes; First oral administration 4 hours after intravenous administration. Esmolol IV infusion at an initial dose of 0.05-0.1 mg / kg / min, followed by a gradual increase in the dose by 0.05 mg / kg / min every 10-15 minutes until an effect or dose of 0.3 mg / kg is achieved. min; for a more rapid onset of the effect, an initial administration of 0.5 mg / kg for 2–5 minutes is possible. Emolol is usually canceled after the second dose of an oral β-blocker, if the correct heart rate and blood pressure were maintained during their combined use.

5) Negative T on baseline ECG (%) 3,451,730,49 (0.12-2.11) "title \u003d" scale (! LANG: GKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Time from onset of symptoms before hospitalization (hours) 5,482.83 ST elevations on baseline ECG (%) 86,293.82.45 (1.13-\u003e 5) Negative T on baseline ECG (%) 3,451,730.49 (0.12-2.11) Scale" class="link_thumb"> 68 !} HKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Time from symptom onset to hospitalization (hours) 5,482,83 ST elevations on baseline ECG (%) 86,293,82.45 (1.13-\u003e 5) Negative T on baseline ECG (%) 3,451,730,49 () GRACE scale: proportion of patients at risk of death \u003d 10% 10,319,42.08 () Killip class I-II (%) 93.193,10.99 () III (%) 5,173, () IV (%) 02, () OKS P ST Data on admission to the hospital RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD) 5) Negative T on baseline ECG (%) 3,451,730.49 (0.12-2.11) Scale "\u003e 5) Negative T on baseline ECG (%) 3,451,730.49 (0.12-2.11) GRACE scale: proportion of patients at risk of death \u003d 10% 10,319,42.08 (0.89-4.88) Killip class I-II (%) 93.193,10.99 (0.35-2.78) III (%) 5,173,860.74 (0.23-2.41) IV (%) 02,741.81 (0.25-13.3) OKS P ST Data on admission to the hospital RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD) "\u003e 5) Negative T on the baseline ECG (%) 3,451,730,49 (0.12-2.11) Scale" title \u003d "(! LANG: GKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Time from symptom onset to hospitalization (hours) 5,482.83 ST elevations on baseline ECG (%) 86,293.82.45 (1.13-\u003e 5) Negative T on baseline ECG (%) 3,451,730 , 49 (0.12-2.11) Scale"> title="HKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Time from symptom onset to hospitalization (hours) 5,482,83 ST elevations on baseline ECG (%) 86,293,82.45 (1.13-\u003e 5) Negative T on the initial ECG (%) 3,451,730,49 (0.12-2.11) Scale"> !}

5 Anticoagulants (%) 81,094,03.69 (1.86-\u003e 5) LMWH (%) 062,4 "title \u003d" (! LANG: GKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Primary reperfusion (%) 27.675.7 Primary PCI (%) 047.9 TLT: Streptokinase (%) 24.15.00.17 (0.09-0.31) T-PA (%) 3.522.8\u003e 5 Anticoagulants (%) 81.094.03.69 (1.86-\u003e 5) NMH (%) 062.4" class="link_thumb"> 69 !} HKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Primary reperfusion (%) 27.675.7 Primary PCI (%) 047.9 TLT: Streptokinase (%) 24.15.00.17 () T-PA (%) 3.522.8\u003e 5 Anticoagulants (%) 81.094.03.69 (1.86-\u003e 5) LMWH (%) 062.4 UFH (%) 10050.5 Fondaparinux (%) 00.1 Bivalirudin (%) 00 , 1 ACS P ST Primary reperfusion therapy and anticoagulant treatment RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD) 5 Anticoagulants (%) 81.094.03.69 (1.86-\u003e 5) LMWH (%) 062.4 "\u003e 5 Anticoagulants (%) 81.094.03.69 (1.86-\u003e 5) LMWH (%) 062.4 UFH (%) 10050, 5 Fondaparinux (%) 00.1 Bivalirudin (%) 00.1 ACS P ST Primary reperfusion therapy and anticoagulant treatment RUSSIAN REGISTER OF ACUTE CORONARY SYNDROMES (RECORD) "\u003e 5 Anticoagulants (%) 81.094.03.69) (1.86-\u003e 5 %) 062.4 "title \u003d" (! LANG: GKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Primary reperfusion (%) 27.675.7 Primary PCI (%) 047.9 TLT: Streptokinase (%) 24,15,00.17 (0.09-0.31) T-PA (%) 3,522,8\u003e 5 Anticoagulants (%) 81,094,03.69 (1.86-\u003e 5) LMWH (%) 062,4"> title="HKB 29 (n \u003d 58) Other centers (n \u003d 1917) Odds ratio (confidence interval) Primary reperfusion (%) 27.675.7 Primary PCI (%) 047.9 TLT: Streptokinase (%) 24.15.00.17 (0.09 -0.31) T-PA (%) 3.522.8\u003e 5 Anticoagulants (%) 81.094.03.69 (1.86-\u003e 5) LMWH (%) 062.4"> !}

Practical approaches in the treatment of AMI Within minutes NPV, heart rate, blood pressure, O 2 saturation ECG monitoring Readiness for defibrillation and CPR Providing IV access 12-lead ECG Short aiming history, physical examination Emergency treatment morphine 2-4 mg in / in until the effect of O l / min to saturate O 2\u003e 90% aspirin (if not given earlier): chew 250 mg, in suppositories 300 mg or in / in 500 mg clopidogrel 300 mg, age 90, if there is pain, acute congestion in the lungs, high blood pressure solution of the issue of TLT !!! 90% aspirin (if not given earlier): chew 250 mg, in suppositories 300 mg or intravenous 500 mg clopidogrel 300 mg, age 90, if there is pain, acute congestion in the lungs, high blood pressure the decision on TLT !!! " \u003e

The term ACS is intended for use by medical personnel performing the initial diagnosis.

ACS is a working term used to describe the totality of symptoms that develop in acute myocardial ischemia. ACS due to myocardial injury - MI. ACS includes the diagnosis of HC, HMBriST, and HMIIST. The term "ACS" is commonly used by nursing staff or emergency room doctors during the initial examination of a patient. The guidelines for making a diagnosis of ACS are given below.

Definition of acute coronary syndrome (ACS)

According to modern terminology, ACS is divided into two large groups based on the applied therapeutic strategy:

1. AMI with ST segment elevation - ACS, in which the patient has typical ischemic chest pain and ST segment elevation is observed. This group of patients immediately after hospitalization needs reperfusion therapy.
2. AMI without ST segment elevation in combination with angina pectoris. ACS, in which patients experience chest pain, and typical ischemic ECG changes in the form of ST elevation are observed transiently or are absent. If biochemical markers of myocardial damage are detected, the condition is regarded as myocardial infarction without ST segment elevation, with a negative result - as unstable angina. This group of patients does not require thrombolytic therapy.

According to the existing classification, there are two main groups that differ in the treatment carried out.

HMnST- ACS, in which the patient has chest pain and ST segment elevation on the ECG. This group of patients should undergo reperfusion.

IMBPvG and NS - ACS, accompanied by the appearance of ischemic discomfort in the patient's chest with transient or permanent ischemic changes. In the presence of biochemical signs of myocardial damage, the condition is called HMBnST, and in their absence, HC. This group of patients does not need thrombolysis.

Causes of Acute Coronary Syndrome (ACS)

These syndromes in most cases occur due to the formation of a blood clot in an atherosclerotic coronary artery. Atherosclerotic plaque becomes unstable, or inflammation processes are activated in it, which causes rupture of the plaque surface, exposure of thrombogenic substances that activate platelets and plasma coagulation factors. As a result, this process ends with the formation of a blood clot. Platelet activation involves conformational changes in the membrane glycoprotein llbllla receptors, as a result of which platelets acquire the ability to bind to each other. Atheomatous changes in the arteries that cause minimal narrowing of the vessel lumen can cause ACS. In more than 50% of patients, the narrowing of the coronary artery is less than 40%. The formed thrombus suddenly creates an obstacle to the delivery of blood to the myocardial site. Spontaneous thrombolysis occurs in about 2/3 of patients, after 24 hours, thrombotic occlusion of the artery is recorded in only 30% of patients. However, in all cases, thrombotic occlusion of the artery lasts a long enough time for the formation of myocardial necrosis.

In more rare cases, these syndromes are the result of coronary embolism. With the use of cocaine and other drugs, spasm of the coronary arteries and MI may develop.

Classification of acute coronary syndrome (ACS)

The classification is based on ECG changes and the presence or absence of cardiac markers in the blood. The separation of HMcST and HM6ST is of practical importance since these conditions differ significantly in terms of prognosis and choice of treatment methods.

Unstable angina is defined as:

• Angina at rest, the attack of which continues long time (usually more than 20 minutes).
• First-onset high FC angina.
• Progressive angina pectoris, the attacks of which have become more frequent, increased the intensity of anginal pain, increased the duration of attacks and decreased the level of threshold load, which provokes the onset of an attack (an increase of more than 1 FC or to the level of minimum PFC).

Symptoms and signs of acute coronary syndrome (ACS)

Clinical manifestations of ACS depend on the localization and severity of changes in the coronary artery and are quite variable.Except when MI is widespread, large-focal, it is difficult to judge the volume of ischemic myocardium based on clinical data alone.

After the completion of acute manifestations of coronary obstruction, complications of the disease may develop. These usually include electrical dysfunction (conduction disturbances, artimia), myocardial dysfunction (heart failure, rupture of the free wall of the LV or IVS, LV aneurysm, pseudoaneurysm, thrombus formation in the LV cavity, cardiogenic shock), or valvular dysfunction (usually manifested as mitral regurgitation ). Violation of the electrical properties of the myocardium is possible with any form of ACS; the appearance of myocardial dysfunction usually indicates a large volume of ischemic myocardium. Other complications of ACS include recurrence of myocardial ischemia and the development of pericarditis. Pericarditis usually develops 2-10 weeks after the onset of myocardial infarction and is known as post-infarction syndrome or Drexler syndrome.

Unstable angina. Symptoms are similar to those for stable angina, with the exception of a few features: attacks are more intense, last longer, are provoked by a lower level of stress, can occur at rest (angina decubitus), progress in their characteristics.

HM6ST and HMcST. The symptoms of HMcST and HM6ST are similar. A few days or weeks before a coronary event, about 2/3 of patients experience prodromal symptoms, which include unstable or progressive angina, shortness of breath, or fatigue. Usually, the first symptom of MI is intense deep chest pain, described by patients as (pressure or it's a dull pain, often radiating to the back, lower jaw, left arm, right arm, shoulders, or all of these areas. According to its characteristics, pain is similar to that of angina pectoris, but usually more intense and prolonged, often accompanied by shortness of breath, sweating, nausea and vomiting, taking nitroglycerin and resting have only a partial and temporary effect. However, the pain syndrome may be less pronounced, about 20% of acute MI are asymptomatic (the clinic is absent or is manifested by nonspecific symptoms that are not perceived by the patient as a disease), which is most often manifested in patients with diabetes mellitus. In some patients, the disease manifests itself as loss of consciousness. Patients often interpret the resulting chest pain as a digestive disorder, partly due to the positive effect after belching and taking antacids. women are characterized by frequent development of an atypical clinic of myocardial infarction. For elderly patients, complaints of dyspnea are more common than anginal pain syndrome. In severe cases, patients experience intense chest pain accompanied by anxiety and fear of death. Nausea and vomiting are possible, the skin is usually pale, cold, damp due to sweating. The appearance of peripheral or central cyanosis is possible.

The appearance of a thread-like pulse, level fluctuations is possible blood pressure, although many patients have arterial hypertension during pain attack.

With the development of RV MI, there is an increase in the filling pressure of the RV, expansion of the jugular veins (often with a positive Kussmaul symptom), the absence of wheezing in the lungs and hypotension.

Diagnostics of the acute coronary syndrome (ACS)

• ECG study in dynamics.
• Study of the level of cardiac markers.
• Coronary angiography for emergency indications in patients with HMcST or its complications.
• Delayed CG for patients with HM6ST or unstable angina.

ACS should be suspected in men over 20 years old and women over 40 years old if they have the main symptoms - chest pain. It is necessary to differentiate anginal chest pain from pain syndrome with pneumonia, rib fracture, costochondral separation, esophageal spasm, acute aortic dissection, nephrolithiasis, splenic infarction. In patients with peptic ulcer or gallbladder disease, it should be noted that the symptoms of ACS will be superimposed on the manifestations of these diseases.

The approach to this category of patients does not differ from the treatment and diagnosis of ACS in the general case: registration and evaluation of ECG in dynamics, investigation of the dynamics of the level of markers of myocardial damage, which makes it possible to differentiate unstable angina, HMcST and HM6ST. Each emergency department should have a triage system for the immediate identification of patients with ACS and ECG recording. In addition to ECG registration, it is necessary to perform pulse oximetry and X-ray examination of the chest organs.

ECG. The ECG is the most important diagnostic test and should be performed within the first 10 minutes of the patient's admission. Based on the analysis of the ECG, one of the most important decisions in the tactics of treating a patient is made - about the introduction of a thrombolytic drug. In the case of HMcST, thrombolytic therapy is indicated, in the case of IMb5, thrombolytic therapy can increase the risk of complications. In addition, for patients with HMcST, emergency CG is indicated, for patients with HM6ST CG may be delayed or performed routinely.

Since non-transmural forms of myocardial infarction (non-O-forming) in most cases affect the subendocardial or mid-myocardial layers of the LV wall, these forms do not form pathological O waves or pronounced ST segment elevation. In contrast, these conditions are characterized by inconsistent and variable changes in the ST segment, which can be non-specific and rather difficult to interpret (MM6ST). If these changes regress (or progress) when analyzing the ECG over time, then the presence of myocardial ischemia is very likely. On the other hand, if the ECG pattern does not undergo regular dynamics, and the diagnosis of myocardial infarction is established on the basis of only clinical data, then it is necessary to confirm the diagnosis using other methods. Registration of a normal ECG in a patient outside of an attack of chest pain does not exclude the diagnosis of unstable angina pectoris, recording a normal ECG in a patient at the height of a pain attack does not exclude the presence of angina pectoris, but indicates a non-ischemic origin of chest pain.

If there is a suspicion of RV MI, a 15-lead ECG is required: additional lead electrodes are placed in the V4R position and for the diagnosis of posterior MI in the V8-V9 position.

Myocardial injury markers. Markers of myocardial damage are cardiac enzymes (CPK-MB) or proteins of the contents of cardiomyocytes, which are released into the systemic circulation during necrosis of cardiomyocytes. Markers of myocardial damage appear in the peripheral blood at different times from the onset of the disease and return to normal at different times.

Usually, various markers of myocardial damage are examined at regular intervals, as a rule, every 6-8 hours during the first day. New techniques make it possible to carry out research directly at the patient's bedside, have sufficient sensitivity for research at shorter intervals.

Troponins are the most specific markers of damage for MI, but their level can also increase in the presence of myocardial ischemia without the development of MI. For each particular laboratory, an upper limit is set for a given test, above which the diagnosis of MI is established. Borderline troponin levels in patients with unstable angina indicate a high risk of adverse events and require more intensive monitoring and treatment. False positive values \u200b\u200bare possible in heart failure and renal failure. The activity level of CPK-MB is less specific. False positive values \u200b\u200bare possible in renal failure, hypothyroidism, and skeletal muscle damage. An increase in the level of myoglobin is nonspecific for MI, however, since its level rises first with the development of MI, this allows one to orient in the choice of treatment tactics in a patient with atypical ECG changes.

Coronary angiography. Coronary angiography is usually performed in conjunction with 4KB. In the case of HMcST, CG is performed on an emergency basis, in addition, CG is indicated if anginal syndrome persists against the background of maximum antianginoal therapy, as well as in patients with the development of complications. Patients with uncomplicated HM6ST or unstable angina pectoris and a good effect on drug treatment CG is usually performed 24-48 hours after hospitalization to determine the coronary artery responsible for the clinic.

After the initial assessment of the patient's condition and the start of drug treatment, CG is performed in case of persistence or recurrence of myocardial ischemia (verified by ECG or clinic data), hemodynamic instability, recurrent ventricular arrhythmias and other manifestations of recurrent ACS.

Other studies. Routine laboratory tests are not diagnostic, but they demonstrate nonspecific changes characteristic of tissue necrosis: accelerated ESR, an increase in the number of leukocytes with a possible shift of the formula to the left. Determination of the blood plasma lipid profile must be performed on an empty stomach in the first 24 hours after the patient is hospitalized.

Radionuclide imaging techniques are usually not used in diagnostics if ECG or marker data are positive. At the same time, echocardiography is absolutely necessary for identifying mechanical complications of myocardial infarction.

Emergency examination should include the following methods

• A quick examination is carried out to exclude hypotension, detect murmurs, and treat acute pulmonary edema.
• A catheter is placed for intravenous access.
• A 12-lead ECG should be recorded and decoded within 10 minutes.
• The patient is prescribed the following drugs:

• Oxygen (start at a concentration of 28% if there is a history of chronic obstructive pulmonary disease).
• Diamorphine for pain relief.
• Metocpopramide for nausea.
• Nitroglycerin spray: 2 inhalations if there is no hypotension.

• They take blood and conduct research:

• Complete blood count and concentration of urea and electrolytes (if necessary, potassium preparations are added to the treatment to maintain its concentration within 4-5 mmol / l).
• The concentration of glucose (can significantly increase in the postinfarction period even in patients without diabetes mellitus, which reflects the release of catecholamines in response to stress, decreases without treatment).
• Biochemical markers of heart damage.
• Lipid metabolism indicators: serum cholesterol and HDL cholesterol remain at the initial level for up to two days, but then decrease, and within 8 weeks or more, their level is restored.

• Plain chest x-ray is done to assess the size of the heart, to detect pulmonary edema, and to exclude mediastinal dilation.
• During the examination, the peripheral pulse should be assessed, the fundus examined, the internal organs should be examined for enlargement of organs and aortic aneurysm.

Acute coronary syndrome (ACS) prognosis

Unstable angina. Severe ECG changes in combination with anginal syndrome are indicators of a high risk of MI and death.

HM6ST and HMcST. The overall mortality rate is about 30%, with 50 to 60% of patients dying in the prehospital phase (usually with advanced ventricular fibrillation).

Most patients with fatal complications of myocardial infarction develop either large-focal myocardial infarction or recurrent myocardial infarction in the presence of a scar in the left ventricle after a previous MI. The development of cardiogenic shock is associated with the involvement of more than 50% of the functioning myocardium in the infarction zone. Five prognostic signs have been established that allow predicting mortality with a probability of up to 90% in patients with HMcST: advanced age (31% of total mortality), decreased systolic blood pressure (24%), heart failure above grade 1 according to Killip (15%), tachycardia (12%), anterior myocardial infarction (6%). There has been an increase in mortality in the presence of diabetes, as well as in women.

Preservation of LV systolic function after MI depends on the amount of remaining functioning myocardium. The presence of scars in the LV after myocardial infarction worsens the patient's prognosis, while in the case of more than 50% of the total myocardial mass, the prognosis is extremely poor.

Primary emergency care for acute coronary syndrome

• If ACS is suspected, continuous ECG monitoring and the possibility of immediate defibrillation should be provided.
• The physician receiving the patient should be instructed on the need to prescribe the patient acetylsalicylic acid (300 mg orally if there are no contraindications) and the undesirability of intramuscular injections [which can lead to an increase in creatine phosphokinase (CPK) levels and provoke bleeding during thrombolytic and anticoagulant therapy].

Mandatory emergency care for ACS

A quick examination to detect hypotension, heart murmurs, and to identify and treat acute pulmonary edema includes the following:

• Providing vascular access - within 10 minutes, 12-lead electrocardiography must be performed and described.

Assign:

• Oxygen therapy (start with 28% oxygen-air mixture if the patient has lung disease).
• Intravenous diamorphization to relieve pain.
• Metoclopramine 10 mg IV if nausea is present.
• Sprays with nitroglycerin twice under the tongue (in the absence of hylotension).

Blood for analysis:

• Urea and electrolytes: maintain the concentration of potassium ions at 4-5 mmol / l.
• Blood glucose: hyperglycemia can be observed from the first hours of signs of heart attack, including in patients without diabetes mellitus, acts as a reflection of stress-induced hypercatecholaminemia and can disappear on its own without treatment.

Biochemical markers of myocardial damage:

• Lipid profile: determination of the level of total cholesterol, long-chain fatty acids, triglycerides. The content of cholesterol, as well as high-density lipoproteins in the blood plasma remains close to normal values \u200b\u200bfor a day or two, then decreases and returns to normal for more than 8 weeks.

Perform in situ x-rays of the cell to determine the size of the heart, the presence of pulmonary edema, and to exclude mediastinal dilation

A general examination includes an assessment of the peripheral pulse, an examination of the fundus, examination of the abdominal organs for hepatosplenomegaly, as well as the presence of an abdominal aortic aneurysm

Conditions that mimic the pain of acute coronary syndrome

• Pericarditis.
• Aortic dissecting aneurysm.
• TELA.
• Esophageal reflux, esophageal spasm or rupture.
• Perforation of a peptic ulcer.
• Pancreatitis

Initial Management of Acute Coronary Syndrome

• All patients with suspected ACS should be monitored continuously by ECG. The room where the patient is located must have all the conditions for defibrillation.
• The referring physician should give the patient aspirin (300 mg by mouth unless contraindicated) and should never be given any intramuscular injection [they cause an increase in total creatine phosphokinase (CPK) and increase the risk of bleeding during thrombolysis / anticoagulation].

Treatment of acute coronary syndrome (ACS)

• Oxygen monitoring and inhalation.
• Bed rest in the first days, then early activation of the patient.
• A diet low in salt and fat.
• Laxatives and sedatives (anxiolytics, tranquilizers) as needed

Treatment is aimed at reducing anxiety, stopping thrombosis, reversing ischemia, limiting the size of myocardial infarction, reducing the load on the myocardium, preventing and treating complications.

Treatment begins at the same time as the diagnosis is made. It is necessary to establish a reliable venous access, oxygen inhalation through nasal cannulas with a flow of 2 liters, continuous ECG monitoring. Interventions at the prehospital stage performed by emergency doctors (ECG registration, aspirin 325 mg - chew, early thrombolysis if indicated and possible, hospitalization of the patient in a specialized hospital) significantly reduce mortality. Early diagnosis and evaluation of the effectiveness of treatment allows you to analyze the needs and time frames for performing myocardial revascularization.

The study of the level of necrosis markers makes it possible to identify groups of patients with low and intermediate risk with suspected ACS (patients with initially negative markers of necrosis and nonspecific ECG changes). Such patients are subject to observation in the next 24 hours in the observation wards. High-risk patients should be admitted to ACS intensive care units equipped with an ECG monitoring system. The most widely used is the TIMI risk assessment system.

Intermediate and high-risk patients with BM65T should be admitted to intensive care units. Patients with MMcST are admitted to the ACS intensive care unit.

Monitoring heart rate and heart rate using a single-channel ECG recording system is in most cases sufficient for routine monitoring. However, some clinicians recommend the use of multichannel ST-offset recording and analysis systems to identify transient recurrent episodes of ST-segment elevation or depression. The detection of such changes, even in patients with no clinical manifestations, indicates the persistence of myocardial ischemia and indicates more aggressive treatment.

Trained nurses can diagnose the development of rhythm disturbances by analyzing the ECG and initiate treatment.

All department staff must have the skills to perform cardiopulmonary resuscitation.

Conditions that complicate the course of myocardial infarction are subject to aggressive treatment.

Treatment should take place in a calm, quiet, relaxing atmosphere. The use of single rooms is preferable, and privacy should be respected in patient visits. Usually, in the first days, visits by relatives and communication by phone are not allowed. Attributes such as wall clock, calendar and window help maintain patient orientation in time and space and avoid feelings of isolation. Listening to radio broadcasts, television and reading newspapers also contribute to this.

In the first 24 hours, bed rest is required. On the first day after myocardial infarction, patients without complications (hemodynamic instability, persistent myocardial ischemia), including patients after reperfusion treatment (fibrinolysis or 4KB), can sit on a chair, begin passive exercises, and use a bedside table. After a while, it is possible to go to the toilet and work with documents in a calm mode. According to recent studies, patients with MI and effective primary 4KB can be transferred to an outpatient regimen early and discharged on the 3-4th day.

Anxiety, frequent mood swings, negative emotions are found in most patients. Mild tranquilizers (usually of the benzodiazepine series) can be used to relieve such phenomena, however, according to experts, the need for their appointment rarely arises.

The development of reactive depression most often occurs on the 3rd day of the disease, with almost all patients suffering depressive disorders during the recovery period. After overcoming the acute phase of the disease, the most important tasks are the treatment of depression, rehabilitation and the development of a long-term prevention program for the patient. Staying too long on bed rest, physical inactivity, and over-focusing on the severity of the illness all contribute to increased anxiety and depressive tendencies. Patients should be encouraged to try to sit up, get up and exercise as early as possible. It is necessary to explain to the patient the nature of the disease, the prognosis and the individual rehabilitation program.

Maintaining normal bowel function with laxatives (such as dokusat) to prevent constipation is an important component of treatment. Urinary retention is also a serious problem, often seen in elderly patients, especially after several days of bed rest and atropine administration. Bladder catheterization may be required in some patients, the catheter can be removed after the patient can get up or sit in bed and empty the bladder on their own.

Since smoking is prohibited in hospitals, the patient's stay in the clinic should be used to stop smoking. All clinic staff in contact with the patient should encourage the patient to quit smoking.

Usually patients in the acute phase of the disease have a significantly reduced appetite, therefore delicious food in moderation, it is more appropriate as a moral support to the patient. In most cases, patients are prescribed a diet of about 1,500-1,800 kcal / day with a reduced Na content to 2-3 g. A decrease in Na intake is not required on the 2-3rd day in the absence of symptoms of heart failure. In addition, the diet should contain a minimum of cholesterol and saturated fat, which is indicative of patient education on healthy eating.

Medications

• Aspirin, clopidogrel, or a combination thereof (prasugrel is an alternative to clopidogrel unless fibrinolytic drugs are prescribed).
• Beta blockers
• Platelet llb / llla receptor blockers are prescribed in the case of 4KB and in some high-risk patients.
• Heparin (unfractionated or low molecular weight) or bivalirudin.
• IV infusion of nitroglycerin (optional in low-risk, uncomplicated MI).
• Fibrinolytic agents for selected groups of patients with HMcST.
• ACE inhibitors (as early as possible) and statins.

Prevention of acute coronary syndrome (ACS)

• Prevention of thrombosis during hospital stay: early mobilization (in uncomplicated cases or after a successful CRP is possible on the 1st day)
• Lifestyle changes: Nicotine withdrawal, regular physical activity, weight loss, blood pressure control
• Low-molecular-weight heparins subcutaneously before hospital discharge (enoxaparin has been studied best of all).
• Platelet aggregation inhibitors:
  • acetylsalicylic acid (ASA): 75-100 mg / day continuously
  • clopidogrel: if ASA is contraindicated or intolerant, clopidogrel should be taken continuously
  • prasugrel: 10 mg / day continuously
• Statins - Onset 1-4 Days Target: Lipoprotein
• Beta-receptor blockers for patients with limited left ventricular function / reduced ejection fraction or tachycardia
• ACE inhibitors - all patients with reduced ventricular function (ejection fraction<40%), сахарным диабетом, гипертонией
• Aldosterone antagonists with high ejection fraction reduction
• An angiotensin receptor antagonist can be tried for ACE inhibitor intolerance and / or signs of heart failure, or limited left ventricular function
• Prevention of sudden cardiac death: in patients with multiple (and persistent) hemodynamically relevant ventricular tachycardias / tachyarrhythmias or in a state after ventricular fibrillation (except for the state 48 hours after coronary syndrome), and especially in the presence of reduced pumping function of the left ventricle, implantation of a cardioverter is indicated. defibrillator.