Acute coronary syndrome treatment at the hospital stage. Treatment of patients with acute coronary syndrome at the prehospital stage. Acute coronary syndrome with ST segment elevation or acute left bundle branch block
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Principles of treatment of unstable angina and non-Q wave MI. The principles of treatment of these conditions are determined by their main similar pathogenetic mechanisms - rupture of atherosclerotic plaque, thrombosis and impaired functional state of the vascular endothelium, and include:
. elimination (prevention) of the consequences of plaque rupture;
. symptomatic therapy.
The main objectives of the treatment of ACS at the prehospital stage are:
1) early diagnosis of heart attack and its complications;
2) pain relief;
3) antiplatelet therapy;
3) prevention and treatment of shock and collapse;
4) Treatment of threatened rhythm disturbances and ventricular fibrillation.
Relief of a pain attack in any manifestation of ACS. Pain from ACS, by affecting the sympathetic nervous system, can negatively affect heart rate, blood pressure and cardiac function. Therefore, it is necessary to stop the pain attack as quickly as possible. The patient should be given nitroglycerin under the tongue, preferably in the form of a spray, this can ease the pain; it can be repeated after 5 minutes. It is not indicated for patients with systolic blood pressure below 90 mm Hg. Art.
At the same time, morphine hydrochloride is administered intravenously in fractions at a dose of 4 to 8 mg; repeated administration of 2 mg can be carried out every 5 minutes until the pain in the chest is completely relieved. The maximum dose is 2-3 mg per 1 kg of patient body weight. Morphine is especially indicated for persistent pain in young, physically strong men who drink alcohol, and in patients with acute heart failure.
Side effects of morphine (hypotension, bradycardia) are extremely rare and can be easily stopped by elevating the legs, administering atropine, and sometimes plasma replacement fluid. In elderly people, depression of the respiratory center is often observed from the administration of morphine, so the drug should be administered to them in a reduced (half) dose and carefully. In these cases, morphine can be replaced with a 1% solution of promedol.
If the respiratory center is depressed, 1-2 ml of 0.5% morphine antagonist, nalorphine, should be administered. Neuroleptoanalgesic drugs (fentanyl and droperidol) are significantly inferior to morphine in pain relief. Promedol in a dose of 10-20 mg (1 ml of 1-2% solution) can be used in patients over 60 years of age, as well as in the presence of concomitant diseases with a bronchospastic component and bradycardia.
It should be noted that at the prehospital stage of the use of drugs in patients with ACS, it is necessary to avoid intramuscular and subcutaneous injections, as well as the administration of drugs orally. The intravenous route of drug administration is preferable and most appropriate in terms of the time of onset of the expected effect and safety.
Antithrombotic therapy
Aspirin inhibits platelet aggregation. It has been proven that aspirin in doses of 75 to 325 mg/day significantly reduces the incidence of death and MI in patients with unstable angina. At the prehospital stage, regular aspirin (but not enteric soluble) should be taken as early as possible; its dose, according to the recommendations of ACC/AAS experts, should be 325 mg, maintenance - 75-100 mg/day. For a faster onset of effect, it should be chewed. It is rapidly absorbed, and therefore its effect on platelets can appear within 20 minutes after administration.The use of ticlopidine at the emergency stage should be considered inappropriate due to the slow onset of the disaggregating effect.
If necessary, oxygen therapy is used through a nasal catheter.
Patients with ACS are subject to immediate and careful hospitalization in a specialized department.
Nesterov Yu.I.
Acute coronary syndrome (ACS) is a group of clinical signs or symptoms that suggest myocardial infarction (MI) or unstable angina (UA).
Classification
Acute coronary syndromes:
1. ACS with ST segment elevation
A) MI with ST segment elevation
Q wave MI
MI without Q wave
B) Prinzmetal's angina
B) Pericarditis
D) Early repolarization syndrome
2.) ACS without ST segment elevation
MI without Q wave
Unstable angina
Treatment tactics depending on the type of ACS
The results of treatment of ACS largely depend on the correct actions of the doctor at the prehospital stage.
The main task of the emergency doctor is to effectively relieve pain and possibly
early reperfusion therapy.
Treatment algorithm for patients with ACS
Sublingual nitroglycerin (0.4 mg) or nitroglycerin aerosol every five minutes. After taking three doses, if chest pain persists and systolic blood pressure is at least 90 mmHg. Art. it is necessary to resolve the issue of prescribing nitroglycerin intravenously as an infusion.
The drug of choice for pain relief is morphine sulfate 10 mg intravenously in a saline sodium chloride solution.
Early administration of acetylsalicylic acid in a dose of 160-325 mg (chew). Patients who have previously taken aspirin can be prescribed clopidogrel 300 mg followed by 75 mg/day.
Immediate administration of β-blockers is recommended for all patients unless there are contraindications to their use (atrioventricular blockade, history of bronchial asthma, acute left ventricular failure). Treatment should begin with short-acting drugs: propranolol at a dose of 20-40 mg or metroprolol (egilok) at 25-50 mg orally or sublingually.
Elimination of factors that increase the load on the myocardium and contribute to increased ischemia: hypertension, cardiac arrhythmias.
Further tactics of providing care to patients with ACS, as already mentioned, are determined by the characteristics of the ECG picture.
Patients with clinical signs of ACS with persistent ST segment elevation or acute left bundle branch block, in the absence of contraindications, should restore the patency of the coronary artery using thrombolytic therapy or primary percutaneous angioplasty.
Whenever possible, thrombolytic therapy (TLT) is recommended to be performed in the prehospital setting. If TLT can be performed within the first 2 hours after the onset of symptoms (especially within the first hour), this can stop the progression of myocardial infarction and significantly reduce mortality. TLT is not performed if more than 12 hours have passed since the anginal attack, with the exception of when ischemic attacks continue (pain, ST segment elevations).
20. Unstable angina (UA)) - the most severe period of exacerbation of coronary artery disease
heart disease (CHD), leading to the development of myocardial infarction (MI) or sudden death. NSC - according to
clinical manifestations and prognostic significance occupies an intermediate position between
the main clinical and morphological forms of IHD are stable angina and acute infarction
myocardium.
Classification of unstable angina (Hamm S.W., Braunwald E.)
All patients with NSC are subject to emergency hospitalization in wards (blocks) for intensive observation and treatment. In parallel with treatment, a dynamic ECG recording, a general blood test, determination of the activity of cardiac-specific enzymes, and, if possible, echocardiography and myocardial scintigraphy are performed. 24-hour clinical and monitoring supervision.
The goals of treatment are to relieve pain, prevent recurrent attacks of angina, and prevent the development of acute myocardial infarction and associated complications. Treatment should begin with aspirin. The antithrombotic effect of ASA is based on the irreversible inhibition of platelet cyclooxygenase. As a result, platelets lose the ability to synthesize thromboxane A2 (TXA2), which induces platelet aggregation and has vasoconstrictor properties. As a result, the possibility of platelet aggregation and thrombus formation is reduced.
If there is coronary pain at the time of admission, the patient is given nitroglycerin 0.5 mg sublingually, after 10-15 minutes. it can be repeated. If the effect is insufficient, neuroleptanalgesia is performed, as in MI. At the same time, intravenous infusions of nitroglycerin and heparin are prescribed. The initial dose of nitroglycerin preparations (1% solution of nitroglycerin, perlinganite, or isosorbitol dinitrate-isoket) is 5-15 mcg/min, then every 5-10 minutes. the dose is increased by 10-15 mcg/min, preventing a decrease in systolic blood pressure less than 100-90 mm. rt. Art.
Beta blockers are important in the treatment of NSC. They help eliminate myocardial ischemia, prevent sudden hemodynamic changes, reduce vascular damage, inhibit the formation of lipid plaques, are preventive agents in relation to the deepening, widening or recurrence of an existing rupture and ruptures of other plaques, and have an antiarrhythmic effect.
The initial use of beta blockers in combination with aspirin and heparin can be used in cases where patients with NSC have hyperactivity of the sympathetic nervous system, manifested by tachycardia, hypertension, and rhythm disturbances. In these cases, beta blockers can be used orally, and intravenous administration may also be recommended.
For spontaneous angina, angina of the Prinzmetal type, calcium antagonists are used, of which the dihydropyridine group - nifedipine - is indicated only for this variant of NSC. In order to relieve an attack of coronary pain, nitroglycerin is given; if it is insufficiently effective, nifedipine is given, asking the patient to chew the tablet for better absorption in the oral cavity. To prevent attacks, nitrates or calcium antagonists are prescribed, preferably long-acting ones (amlodipine, Lomir, etc.); verapamil and dilgiazem can be used. Beta blockers in the “pure” vasospastic form of NSC can worsen coronary blood flow. Beta blockers are considered contraindicated in those patients with spontaneous angina in whom spasm of the large coronary arteries is documented on coronary angiography using an ergometrine test.
In cases where by the time of hospitalization there is no evidence of progression of NSC, especially when the last attack of angina was 48 hours later, there are no changes on the ECG, there is no increase in cardiac-specific enzymes, treatment may be limited to aspirin in combination with beta blockers, and/ or nitrates. In some cases, calcium antagonists can be used - veripamil, diltiazem, but not nifedipine. Especially in cases where beta blockers are contraindicated. These calcium antagonists can be combined with nitrates.
If the heart rhythm is disturbed, antiarrhythmic treatment is carried out, including electropulse therapy.
In cases where, within 48-72 hours, despite active therapy, angina attacks do not change in intensity and duration, there are indications for urgent coronary angiography and discussion of the issue of surgical treatment.
An alternative to surgical treatment of NSC is currently PTCA and intracoronary prosthetics using intravascular prostheses (stents). Indications for its implementation are proximal single-vessel stenoses of at least 50% of the vessel lumen
Thus, the sequence of therapeutic measures in the treatment of NSC can be presented as follows: hospitalization in an intensive care unit, prescription of aspirin, nitroglycerin, heparin, beta blockers; for vasospastic variants of NSC - nitroglycerin, calcium antagonists; in acute coronary syndrome with ST segment elevation or fresh left bundle branch block - the use of thrombolytic drugs. In the future, the use of platelet glycoprotein receptor blockers II beta/III alpha and low molecular weight heparins. If drug therapy is ineffective, surgical treatment (CABG, PTCA, intracoronary prosthetics - stents) is recommended. Next, transition to planned treatment according to generally accepted methods for chronic ischemic heart disease.
21. Myocardial infarction (MI) – This is an acute focal necrotic lesion of the heart muscle.
Risk factors
Tobacco smoking and passive smoking, arterial hypertension, increased concentration
LDL cholesterol ("bad" cholesterol) in the blood, low concentration of HDL cholesterol
("good" cholesterol) in the blood, high levels of triglycerides in the blood, low levels of physical
activity, age, air pollution, men are more likely to suffer from myocardial infarction than
women, obesity, Alcoholism, Diabetes mellitus, Previous myocardial infarction and manifestation
any other manifestations of atherosclerosis
CLASSIFICATION
By stages of development:
Prodromal period (0-18 days)
The most acute period (up to 2 hours from the onset of MI)
Acute period (up to 10 days from the onset of MI)
Subacute period (from 10 days to 4-8 weeks)
Scarring period (from 4-8 weeks to 6 months)
According to the anatomy of the lesion:
Transmural
Intramural
Subendocardial
Subepicardial
By volume of damage:
Large-focal (transmural), Q-infarction
Small focal, non-Q infarction
Localization of the necrosis focus.
Myocardial infarction of the left ventricle (anterior, lateral, inferior, posterior).
Isolated myocardial infarction of the apex of the heart.
Myocardial infarction of the interventricular septum (septal).
Right ventricular myocardial infarction.
Combined localizations: posteroinferior, anterolateral, etc.
With the flow:
Monocyclic
Lingering
Recurrent myocardial infarction (in the 1st coronary artery, a new focus of necrosis occurs from 72 hours to 8 days)
Repeated MI (in another cor. art., a new focus of necrosis 28 days after the previous MI)
Clinical classification prepared by a joint working group of the European Society of Cardiology, the American College of Cardiology, the American Heart Association and the World Heart Federation (2007):
Spontaneous MI (Type 1) associated with ischemia due to a primary coronary event, such as plaque erosion and/or rupture, cracking, or dissection.
Secondary myocardial infarction (type 2), associated with ischemia caused by increased oxygen deficiency or supply,
Sudden coronary death (type 3), including cardiac arrest,
PCI-associated MI (type 4a).
MI associated with stent thrombosis (type 4b), which is confirmed by angiography or autopsy.
CABG-associated MI (type 5).
Pathogenesis
There are stages:
1) Ischemia 2) Damage (necrobiosis) 3) Necrosis 4) Scarring
Ischemia can be a predictor of heart attack and last for quite a long time. The process is based on a violation of myocardial hemodynamics. Usually, narrowing of the lumen of the artery of the heart to such an extent that the restriction of blood supply to the myocardium can no longer be compensated is considered clinically significant. Most often this occurs when the artery is narrowed by 70% of its cross-sectional area. When compensatory mechanisms are exhausted, they speak of damage, then the metabolism and function of the myocardium suffer. The changes may be reversible (ischemia). The damage stage lasts from 4 to 7 hours. Necrosis is characterized by irreversible damage. 1-2 weeks after a heart attack, the necrotic area begins to be replaced by scar tissue. The final formation of the scar occurs after 1-2 months.
22. Clinical picture of acute MI. The most typical manifestation of myocardial infarction is chest pain. The pain “radiates” along the inner surface of the left arm, producing a tingling sensation in the left hand, wrist, and fingers. Other possible areas of irradiation are the pleural girdle, neck, jaw, interscapular space, also predominantly on the left. Thus, both the localization and irradiation of pain do not differ from an attack of angina.
The pain during myocardial infarction is very strong, perceived as dagger-like, tearing, burning, “a stake in the chest.” Sometimes this feeling is so unbearable that it makes you scream. Just as with angina pectoris, there may be not pain, but discomfort in the chest: a feeling of strong compression, squeezing, a feeling of heaviness “pulled with a hoop, squeezed in a vice, pressed down with a heavy slab.” Some people experience only a dull ache or numbness in the wrists combined with severe and prolonged chest pain or chest discomfort.
The onset of anginal pain during myocardial infarction is sudden, often at night or in the early morning hours. Painful sensations develop in waves, periodically decrease, but do not stop completely. With each new wave, pain or discomfort in the chest intensifies, quickly reaches a maximum, and then weakens.
An attack of pain or discomfort in the chest lasts more than 30 minutes, sometimes for hours. It is important to remember that for the formation of myocardial infarction, a duration of anginal pain of more than 15 minutes is sufficient. Another important hallmark of myocardial infarction is the lack of reduction or cessation of pain at rest or when taking nitroglycerin (even repeatedly).
Clinical options for myocardial infarction:
asthmatic variant characterized by the development of an attack of cardiac asthma or pulmonary edema (see the corresponding section). It occurs more often in older patients;
gastralgic(abdominal) variant begins with pain in the epigastrium and behind the sternum, nausea, and possibly vomiting. Sometimes the pain radiates to the lower abdomen, and signs of dynamic intestinal obstruction may appear. It can be especially difficult to recognize this type of myocardial infarction in patients with a history of gastric and duodenal ulcers. However, palpation of the abdomen in this case does not cause significant pain, the abdomen is soft, there are no symptoms of peritoneal irritation, which does not correspond to the patient’s complaints of very severe pain. (Just don’t forget that myocardial infarction and acute surgical diseases can occur simultaneously!);
cerebral This variant manifests itself as an acute cerebrovascular accident. Loss of consciousness, epileptiform convulsions, speech impairment, paresis and paralysis may occur. This can be explained by both the simultaneous development of myocardial infarction and stroke (vasospasm or blood clots simultaneously entering the vessels of the heart and brain), and complications of myocardial infarction, for example, Morgagni-Adams-Stokes syndrome (arrhythmia), which caused brain hypoxia;
arrhythmic option - the emergence for the first time of various rhythm and conduction disorders;
painless(atypical) variant of myocardial infarction is manifested only by changes on the ECG, sometimes detected by chance.
23. ECG : In the most acute stages (stages of damage, most often from 20 minutes to 2 hours) - in the ECG leads recorded over the area of infarction - a monophasic curve: the ST segment is sharply raised above the isoline, forms an arc, convex upward, merging directly with a high positive T wave. In an acute stage of MI, which lasts up to 10 days (usually one week), a focus of necrosis is formed. At the same time, the ECG registers pathological deep and wide Q wave and The R wave decreases. The deeper and wider the Q wave, the smaller the R wave, and with transmural infarction the wave R at all disappears. The ST segment begins to gradually decline, but remains above the isoline, and the tooth T becomes negative. In leads opposite to the localization of MI, the ECG records reciprocal changes. In the acute period of MI they are the opposite of the main ones. In subacute stage in the leads recorded above the MI area, the QRS complex remains the same, as in the acute stage, the ST segment is close to the isoelectric line, the T wave is deep, negative, equilateral ("coronary" Purdy wave). The duration of this stage is 4-5 weeks.
During the scarring stage, the QRS complex remains the same as in the subacute stage, but after a year or more, the pathological Q wave may decrease or even disappear, and the voltage of the R wave may increase slightly. This is explained by compensatory hypertrophy of the myocardium in the scar area. The ST segment is on the isoelectric line, T becomes less negative, or smoothed, or even slightly positive. The duration of this stage is on average 8 weeks or more from the onset of myocardial infarction. The main sign of the scar stage is the absence of further ECG dynamics.
Laboratory data
Within a few hours after the development of MI, the number of leukocytes in the blood increases and persists for 3-7 days, mainly due to neutrophils (shift of the leukocyte formula to the left). The first days of the disease are characterized by a decrease in the number of eosinophils up to aneosinophilia. ESR remains normal in the first days and begins to increase after 1-2 days, after the temperature rises and the number of leukocytes increases. By the end of the week, leukocytosis decreases and ESR increases (“scissors symptom”). The maximum ESR is usually observed between the 8th and 12th day of illness, then gradually decreases and returns to normal after 3-4 weeks.
The most valuable method for laboratory diagnosis of MI– study of the activity of blood serum enzymes. An early and informative diagnostic test is the determination of troponin-T. It appears after 6-8 hours, reaches a maximum after 24-36 hours and remains elevated for 10-14 days.
The activity of creatine phosphokinase (CPK), especially its isoenzyme MB, increases. It is observed within 6-8 hours from the onset of MI and normalizes within 2-3 days. Aminotransferases (especially AST and to a lesser extent ALT) increase. In AST, the initial increase is observed after 8-12 hours, the maximum increase is on the 2nd day and normalizes by 3-7 days. The activity of lactate dehydrogenase (especially the first isoenzyme - LDH 1) increases 24-48 hours from the onset of the disease, the maximum increase is by 3-5 days and normalizes by 8-15 days. The content of sialic acids and C-reactive protein in the blood serum also increases, which remain at elevated levels for up to 2 weeks.
Widely used for diagnosing myocardial infarction myoglobin in the blood, which normally does not exceed 85 ng/ml. An important advantage of this test is its earlier appearance: on average 2-3 hours earlier than the increase in the activity of the “earliest” enzyme – CPK-MB.
Of other additional diagnostic methods, radioisotope research methods have the greatest “resolving” ability, in particular, scintigraphy with technetium and thalium . It allows you to diagnose MI where other methods are powerless.
Treatment of MI
1. Relief of pain syndrome.
2. Restoration of coronary blood flow.
3. Reducing heart work and myocardial oxygen demand.
4. Limiting the size of myocardial infarction.
5. Treatment and prevention of complications of myocardial infarction.
1.Morphine intravenously in fractions
Adequate pain relief, reduction of pre- and afterload, psychomotor agitation, myocardial oxygen demand (2-5 mg intravenously every 5-15 minutes until pain is completely eliminated or until side effects appear)
2.C Treptokinase (streptase)
Restoration of coronary blood flow (thrombolysis), relief of pain, limitation of the size of myocardial infarction, reduction of mortality (1.5 million IU intravenously in 60 minutes)
3.Heparin intravenous bolus (if thrombolysis is not performed) Prevention or limitation of coronary thrombosis, prevention of thromboembolic complications, reduction of mortality (10,000-15,000 IU intravenous bolus)
4. Nitroglycerin or isosorbide dinitrate intravenous drip. Relief of pain, reduction in the size of myocardial infarction and mortality (10 mcg/min. with an increase in speed by 20 mcg/min every 5 minutes under the control of heart rate and blood pressure_
5. Beta blockers: propranolol (obzidan) Reducing myocardial oxygen demand, relieving pain, reducing the size of necrosis, preventing ventricular fibrillation and left ventricular rupture, repeated myocardial infarction, reducing mortality (1 mg/min every 3-5 minutes to a total dose of 10 mg)
6. Acetylsalicylic acid (aspirin) Relief and prevention of processes associated with platelet aggregation; with early(!) administration, it reduces mortality (160-325 mg chewed;)
7. Magnesium sulfate (cormagnesin) Reducing myocardial oxygen demand, relieving pain, reducing the size of necrosis, preventing cardiac arrhythmias, heart failure, reducing mortality (1000 mg magnesium (50 ml 10%, 25 ml 20% or 20 ml 25% solution) intravenously for 30 minutes.)
Acute coronary syndrome (for simplicity it is abbreviated as ACS) is a working diagnosis used by emergency and ambulance doctors. In fact, it combines two diseases - unstable angina and true myocardial infarction.
We recommend reading:Causes of acute coronary syndrome
The main cause of ACS was and remains atherosclerosis. Deposits in the form of plaques on the walls of the coronary arteries lead to a narrowing of the effective lumen of the vessels. Partial destruction of the plaque capsule provokes parietal thrombus formation, which further impedes blood flow to the heart muscle. A decrease in the capacity of the coronary artery by more than 75% leads to the appearance of symptoms of myocardial ischemia. According to this mechanism, unstable angina pectoris develops more often - a more favorable form of ACS.
The second mechanism is the complete detachment of the plaque and its blockage of the coronary arteries. In this case, the blood flow completely stops and the phenomena of ischemia and, later, necrosis rapidly increase in the heart muscle. Myocardial infarction develops.
The third mechanism is the occurrence of a powerful spasm of the coronary arteries under the influence of catecholamines released in response to stress. The process that occurs as a result of taking certain medications with a vasoconstrictor effect is also similar.
Symptoms of the disease
The main clinical symptom of ACS is chest pain, varying in both intensity and sensation. It can be squeezing, pressing, burning - these are the most typical forms of pain. An attack of ischemia is provoked by stress, physical activity, emotional stress, and taking certain medications and drugs (amphetamines, cocaine).
Often it is not localized only behind the sternum, but radiates to various regions of the body - neck, left arm, shoulder blade, back, lower jaw. Situations are possible when pain is felt exclusively in the upper abdomen, simulating the clinical picture, for example, of acute pancreatitis. In this case, the diagnosis is facilitated by instrumental and laboratory studies. However, the abdominal form of myocardial ischemia still remains the most difficult to diagnose.
The second most common symptom is shortness of breath. Its occurrence is associated with a decrease in the functions of the heart in pumping blood. The appearance of this clinical sign indicates a high probability of life-threatening acute heart failure with pulmonary edema.
The third symptom is the occurrence of various arrhythmias. Sometimes heart rhythm disturbances are the only sign of an impending myocardial infarction, which can occur in a painless form. In this case, there is also a high risk of developing fatal complications in the form of cardiac arrest or cardiogenic shock, followed by the death of the patient.
How is ACS detected?
Prehospital physicians are extremely limited in the means of diagnosing acute coronary syndrome. Therefore, they are not required to make an accurate diagnosis. The main thing is to correctly interpret the data available at the time of examination and transport the patient to the nearest medical center for final identification of the disease, observation and treatment.
An emergency physician or therapist suspects ACS based on:
- medical history data (what could have provoked the attack, whether it was the first, when the pain occurred and how it developed, whether the pain was accompanied by shortness of breath, arrhythmia and other signs of ACS, what medications the patient took before the attack);
- data from listening to heart sounds, blood pressure numbers;
- electrocardiographic study data.
However, the main diagnostic criterion is the duration of chest pain. If the pain lasts more than 20 minutes, the patient is given a preliminary diagnosis of ACS. Depending on the ECG signs, it can be supplemented with information about the presence or absence of ST segment elevation.
Emergency care for acute coronary syndrome
The patient's chances of survival are higher the faster he receives emergency care for acute coronary syndrome. Even if ACS subsequently develops into myocardial infarction, timely medical intervention will limit the area of necrosis and reduce the consequences of the disease.
WHO proposes the following algorithm for carrying out emergency measures:
- The patient is placed on his back, the clothes on his chest are unbuttoned;
- the most important element of treatment is oxygen therapy, which promotes the saturation of myocardial cells with oxygen under conditions of tissue hypoxia;
- administration of nitroglycerin under the tongue at intervals of 5 minutes, three doses, taking into account contraindications;
- give aspirin in a dose of 160-325 mg once;
- anticoagulants are administered subcutaneously - heparin, fondaparinux, fraxiparin, etc.;
- analgesia with morphine in a dose of 10 mg is required with a single repeat of the same amount of the drug after 5-15 minutes if necessary;
- oral administration of one of the drugs from the beta-blocker group is prescribed, taking into account contraindications (low blood pressure, bradyarrhythmia).
In addition to these measures, actions are taken to eliminate complications, such as arrhythmias, impending or existing pulmonary edema, cardiogenic shock, etc.
After stabilizing the patient’s condition, he is urgently hospitalized in a hospital where there are conditions for thrombolysis (destruction of a blood clot), and if there is no such medical institution within reach, in any hospital with an intensive care unit or intensive care unit.
It should be remembered that the patient’s life depends on timely emergency care provided at the prehospital stage. World practice shows that most deaths from myocardial infarction occur before the arrival of specialized medical teams. For this reason, any patient with coronary heart disease should be trained in both recognizing the first signs of acute coronary syndrome and self-help tactics when an attack begins.
Module 7ACUTE CORONARY SYNDROME: EMERGENCY MEDICAL CARE AT THE PREHOSPITAL STAGE
I. GENERAL CONCEPTS
Definition. Acute coronary syndrome (ACS) is a group of clinical signs or symptoms that make it highly likely to suspect myocardial infarction (MI) or unstable angina (UA) upon first contact with the patient. ACS includes conditions caused by acute ischemic changes in the myocardium: UA (new or progressive), non-ST segment elevation MI (STEMI) and ST-segment elevation MI (STEMI).
At the prehospital stage of emergency medical care (DE EMS), differential diagnosis between UA and STEMI is not carried out. Since at an early stage of diagnosis (including in a hospital) it is not always possible to differentiate between NS and MI, as well as other diseases with a similar clinical picture, it is advisable to distinguish between “probable ACS”, as a preliminary diagnosis during emergency hospitalization of the patient, and “suspected ACS” , as a secondary diagnosis in cases where another disease is the more likely cause of treatment, but ACS has not yet been excluded. It should be noted that overdiagnosis of ACS at the prehospital stage is a smaller error than underestimating the patient’s condition. In a third of cases, ACS may have an atypical course.
To assess the clinical situation, E. Braunwald (1989) proposed subdividing unstable angina according to the severity of clinical manifestations and the conditions for the occurrence of attacks as follows (Table).
Classification of unstable angina (according to E. Braunwald, 1989)
Etiology and pathogenesis. Possible causes of an acute decrease in coronary blood flow may be prolonged spasm of the coronary vessels, a sharp increase in myocardial oxygen demand, thrombotic changes against the background of stenosing sclerosis of the coronary arteries and damage to the atherosclerotic plaque, as well as hemorrhage into the plaque and intimal detachment of the artery.
The formation of coronary artery occlusion leads to insufficient oxygen supply to the myocardium with subsequent formation of necrosis of the heart muscle. Moreover, the longer the period of ischemia lasts, the greater the area and depth of necrosis. After 4-6 hours of ischemia, the zone of necrosis of the heart muscle practically corresponds to the area of the blood supply to the affected vessel.
Acute coronary syndrome (ACS)– any group of clinical signs or symptoms that suggest myocardial infarction or unstable angina.
ST segment elevation- as a rule, a consequence of transmural myocardial ischemia and occurs with the development of complete occlusion of the main coronary artery.
In cases where ST elevation is short-term, transient in nature, we may be talking about vasospastic angina ( Prinzmetal's angina).
Such patients also require emergency hospitalization, but are subject to the management of ACS without persistent ST elevation. In particular, thrombolytic therapy is not performed.
Persistent ST segment elevation lasting more than 20 minutes is associated with acute complete thrombotic occlusion of the coronary artery.
OKC with ST rise diagnosed in patients with an anginal attack or chest discomfort and changes in the form of persistent ST segment elevation or “new”, i.e. for the first time (or presumably for the first time) a complete block of the left bundle branch (LBB) occurred on.
ACS is a working diagnosis, used in the first hours and days of the disease, while the terms myocardial infarction (MI) and unstable angina (UA) are used to formulate the final diagnosis, depending on whether signs of myocardial necrosis are identified.
The diagnosis of MI is made based on the following criteria:
- 1. Significant increase in biomarkers of cardiomyocyte necrosis in combination with at least one of the following signs:
- symptoms of ischemia,
- episodes of ST segment elevation or new complete blockade of the left bundle branch,
- the appearance of a pathological Q wave on,
- the appearance of new zones of impaired local myocardial contractility,
- detection of intracoronary thrombosis during, or detection of thrombosis during autopsy.
Detection of ischemic changes on the electrocardiogram allows you to avoid errors in choosing medical tactics.
2.2. Asthmatic variant is a manifestation of acute left ventricular failure in the form of an attack of cardiac asthma or pulmonary edema and is usually observed in elderly patients, usually with pre-existing organic heart disease.
Chest discomfort does not correspond to classic characteristics or may be practically absent.
2.3. Arrhythmic variant characterized by predominant manifestations of rhythm and conduction disturbances, while the pain syndrome is absent or slightly expressed. The identification of electrocardiographic changes of an ischemic nature is of decisive importance.
2.4. Cerebrovascular variant occurs in elderly patients, with a history of strokes or with severe chronic cerebrovascular accidents.
The presence of intellectual-mnestic disorders or acute neurological pathology often does not allow us to assess the nature of the pain syndrome in the chest.
Clinically, the disease manifests itself with neurological symptoms in the form of dizziness with nausea, vomiting, fainting or cerebrovascular accident.
Considering that severe strokes, even without the development of myocardial infarction, can be accompanied by infarct-like changes in blood pressure, the decision on the administration of thrombolytics or antithrombotic drugs should be postponed until the results of imaging studies are available.
In other cases, the patient management algorithm is determined by the nature of electrocardiographic changes.
2.5. Painless form Myocardial infarction is more often observed in patients with diabetes mellitus, in the elderly, and after a previous heart attack or stroke.
The disease is discovered as an incidental finding during imaging or echocardiographic examination, sometimes only at autopsy.
Some patients, when questioned, do not describe chest discomfort as pain, or do not attach importance to the increase in short-term attacks of angina, while this may be a manifestation of a heart attack.
The perception of anginal pain can be disrupted by depression of consciousness and the administration of painkillers during strokes, injuries and surgical interventions.
In any case, even suspicion of ACS in such patients should be grounds for immediate hospitalization.
It should be borne in mind that normal or slightly changed does not exclude the presence of ACS and therefore, in the presence of clinical signs of ischemia, the patient requires immediate hospitalization.
During follow-up (monitoring or re-registration), typical changes can be recorded later.
The combination of severe pain and persistently normal pain makes it necessary to carry out a differential diagnosis with other, sometimes life-threatening conditions.
The role of rapid determination of troponins increases when the clinical picture is unclear and initially altered.
At the same time, a negative result should not be a basis for refusing urgent hospitalization with suspected ACS.
Echocardiography may help make a diagnosis in certain situations, but should not delay hospitalization. (IIb, C). This study is practically not performed by the emergency medical team, and therefore cannot be recommended for routine use.
DIFFERENTIAL DIAGNOSTICS
Differential diagnosis of STEMI should be carried out with pulmonary embolism, aortic dissection, acute pericarditis, pleuropneumonia, pneumothorax, intercostal neuralgia, disease of the esophagus, stomach and duodenum (peptic ulcer), other organs of the upper abdominal cavity (diaphragmatic hernia, hepatic colic with bile ducts). stone disease, acute cholecystitis, acute pancreatitis).
TELA – the clinic is dominated by sudden shortness of breath, which is not aggravated in a horizontal position, accompanied by pallor or diffuse cyanosis.
The pain syndrome may resemble angina. In many cases, there are risk factors for venous thromboembolism.
At esophageal spasm chest pain can resemble ischemic pain, often relieved with nitrates, but can also go away after a sip of water. However, it does not change.
Diseases of the upper abdominal organs usually accompanied by various manifestations of dyspepsia (nausea, vomiting) and abdominal pain on palpation.
A perforated ulcer can simulate a heart attack, so during examination the abdomen should be palpated, paying special attention to the presence of symptoms of peritoneal irritation.
It should be emphasized that in the differential diagnosis of these diseases, it is of utmost importance.
Choice of treatment tactics
Once the diagnosis of NSTE-ACS is established, it is urgent to determine the tactics of reperfusion therapy, i.e. restoration of patency of an occluded coronary artery.
Reperfusion therapy (PCI or thrombolysis) is indicated for all patients with chest pain/discomfort of lasting<12 ч и персистирующим подъемом сегмента ST или новой блокадой левой ножки пучка Гиса (I,A).
- If ischemia persists or pain and changes recur, reperfusion therapy (preferably PCI) is performed even if symptoms develop > 12 hours (I, C).
- If more than 24 hours have passed since the onset of symptoms and the condition is stable, routine PCI is not planned (III, A).
- In the absence of contraindications and the impossibility of performing PCI within the recommended time frame, thrombolysis is performed (I, A), preferably at the prehospital stage.
- Thrombolytic therapy is performed if PCI cannot be performed within 120 minutes of first contact with a health care provider (I, A).
- If it has been less than 2 hours since the onset of symptoms and PCI cannot be performed within 90 minutes, thrombolytic therapy should be given if the infarction is large and the risk of bleeding is low (I, A).
- After thrombolytic therapy, the patient is sent to a center with the possibility of performing PCI (I, A).
Absolute contraindications to thrombolytic therapy:
- Hemorrhagic stroke or stroke of unknown origin of any date
- Ischemic stroke in the previous 6 months
- Brain trauma or tumors, arteriovenous malformation
- Major trauma/surgery/trauma within the previous 3 weeks
- Gastrointestinal bleeding within the previous month
- Established bleeding disorders (excluding menses)
- Aortic wall dissection
- Non-compressible puncture (including liver biopsy, lumbar puncture) in the previous 24 hours
Relative contraindications:
- Transient ischemic attack within the previous 6 months
- Oral anticoagulant therapy
- Pregnancy or postpartum condition within 1 week
- Resistant hypertension (systolic blood pressure >180 mm Hg and/or diastolic blood pressure >110 mm Hg)
- Severe liver disease
- Infective endocarditis
- Exacerbation of peptic ulcer
- Prolonged or traumatic resuscitation
Drugs for thrombolysis:
- Alteplase (tissue plasminogen activator) 15 mg IV as a bolus of 0.75 mg/kg over 30 minutes, then 0.5 mg/kg over 60 minutes IV. The total dose should not exceed 100 mg
- Tenecteplase- once intravenously as a bolus depending on body weight:
30 mg -<60 кг
35 mg - 60-<70 кг
40 mg - 70-<80 кг
45 mg - 80-<90 кг
50 mg - ≥90 kg
In all patients with ACS, in the absence of contraindications, dual antiplatelet therapy is indicated ( I , A ):
If primary PCI is planned:
- Aspirin 150-300 mg orally or 80-150 mg intravenously if oral administration is not possible
- Clopidogrel orally 600 mg (I,C). (If possible, Prasugrel 60 mg (I,B) or Ticagrelor 180 mg (I,B) is preferred in clopidogrel-naïve patients under 75 years of age (I,B)).
If thrombolysis is planned:
- Aspirin 150-500 mg orally or 250 mg intravenously if oral administration is not possible
- Clopidogrel orally at a loading dose of 300 mg if age ≤75 years
If neither thrombolysis nor PCI is planned:
- Aspirin orally 150-500 mg
- Clopidogrel orally 75 mg
Other drug therapy
- Opioids intravenously (morphine 4-10 mg), in elderly patients must be diluted in 10 ml of saline and administered in 2-3 ml increments.
If necessary, additional doses of 2 mg are administered at intervals of 5-15 minutes until pain is completely relieved). Side effects may develop: nausea and vomiting, arterial hypotension with bradycardia and respiratory depression.
Antiemetics (eg, metoclopramide 5-10 mg intravenously) can be administered concomitantly with opioids.
Hypotension and bradycardia are usually treated with atropine at a dose of 0.5-1 mg (total dose up to 2 mg) intravenously;
- Tranquilizer (Diazepam 2.5-10 mg IV) if severe anxiety occurs
- Beta blockers in the absence of contraindications (bradycardia, hypotension, heart failure, etc.):
Metoprolol - in case of severe tachycardia, preferably intravenously - 5 mg every 5 minutes for 3 injections, then after 15 minutes 25-50 mg under the control of blood pressure and heart rate.
In the future, tablet drugs are usually prescribed.
- Nitrates for pain sublingually: Nitroglycerin 0.5-1 mg tablets or Nitrospray (0.4-0.8 mg). For recurrent angina and heart failure
Nitroglycerin is administered intravenously under blood pressure control: 10 ml of a 0.1% solution is diluted in 100 ml of saline.
Constant monitoring of heart rate and blood pressure is necessary, do not administer if systolic blood pressure decreases<90 мм рт. ст.
Oxygen inhalation (2-4 l/min) in the presence of shortness of breath and other signs of heart failure
PROVISION OF EMERGENCY MEDICAL CARE AT THE HOSPITAL STAGE IN THE INPATIENT EMERGENCY DEPARTMENT (STEMS)
Patients with ACS with pST should be immediately referred to the ICU.
When presenting the material, the classes of recommendations and levels of evidence proposed by the ACC/AHA and used in the Russian recommendations were used.
ClassIIA- Available evidence is more likely to support the benefit and effectiveness of a diagnostic or treatment method
