Лечение острейшего периода инфаркта миокарда

[Algor]

Уважаемые доктора!
Хотел бы проконсультироваться у кардиологов, как у узких специалистов, по поводу применения адреналина в острейшем периоде инфаркта миокарда. Вышел у меня недавно спор с анестезиологом по этому поводу, вот я и хочу разобраться. Как я понимаю, адреналин резко увеличивает потребность миокарда в кислороде, поэтому не может быть рекомендован даже при кардиогенном шоке?
Если не сложно, выскажитесь пожалуйста по этому поводу, желательно с ссылками, в т.ч. на англоязычные ресурсы. Хотелось бы услышать позицию по этому вопросу доказательной медицины. Также поделитесь собственным мнением, случаями из практики и т.д.

[Dr.]

[Ссылки доступны только зарегистрированным пользователям ]

Если интересно - вот еще из Current Diagnosis & Treatment in Cardiology 2nd Ed:

B. GENERAL PROCEDURES

1. Intravenous line— An intravenous line should be placed immediately in any patient who is seriously considered to have suffered acute ischemia; this will provide access for the administration of pharmacologic agents should they be necessary and for emergency treatment should the need arise. The IV line should be large (18 gauge or greater); its patency should be maintained with an infusion of 5% dextrose in water, one-half normal saline, or normal saline solution.
2. Oxygen— Oxygen is appropriate for all patients with suspected AMI. Given the current aggressive approach toward anticoagulation and reperfusion in treating coronary heart disease, which often entails the use of potent anticoagulants or thrombolytic agents, blood gas determinations are not appropriate as a routine measure; oximetry is preferred. The empiric use of oxygen, usually via nasal prongs at 2–4 L/min, is recommended for all patients except those who have both normal oxygen saturations by oximetry or some reason to withhold oxygen (eg, a history of CO2 retention). Even patients with severe chronic obstructive pulmonary disease who may be at risk for CO2 retention should receive oxygen if systemic oxygenation is inadequate. Although supported by experimental data, the concern that supraphysiologic doses of oxygen may induce vasoconstriction and adverse effects has never been convincingly documented clinically.
3. Relief of discomfort— Relief of discomfort is a high priority.
a. Sublingual nitroglycerin— Unless contraindicated by hemodynamic abnormalities, sublingual nitroglycerin can be used to try to relieve chest discomfort and reverse ECG changes. A reversal of ECG changes is found most often in patients with patent infarct-related coronary arteries; it suggests that ischemia rather than infarction is present. Nitroglycerin must be given cautiously, however, especially to patients with inferior MI who may have RV infarction and who are prone to hypotension in response to this agent. A small subset of patients without RV infarction will also develop hypotension and an inappropriately slow heart rate after nitroglycerin. This is a vagally mediated phenomenon that has also been reported with morphine sulfate. Atropine (0.5 mg) is the treatment of choice in such cases.
b. Intravenous nitroglycerin— If patients have a beneficial response to sublingual nitroglycerin, it is reasonable to initiate treatment with IV nitroglycerin at a low dose (5–10 µg/min). Although this may relieve some of the chest discomfort in patients with acute infarction, it does not reduce the need for treatment with analgesics. Furthermore, reductions in blood pressure by more than 10% in normotensive patients are likely to be detrimental. Keeping the dose low and not expecting it to provide total relief of discomfort is recommended. This approach reduces the incidence of tolerance to the agent, which occurs in up to 25% of patients. Some physicians also use more potent vasodilators such as sublingual nifedipine to assess whether chest pain can be relieved and ECG changes reversed. Although these agents are effective, there is an associated incidence of marked hypotension that can cause detrimental cardiovascular effects. Calcium channel blockers are not recommended for routine administration.
c. Morphine sulfate— If the patient does not have a prompt response to sublingual nitroglycerin, morphine sulfate is the drug of choice. An IV dose of 2–4 mg and repeated as necessary and tolerated until chest discomfort is relieved is recommended. In addition to relieving pain, morphine sulfate reduces anxiety and the catecholamine secretion that occurs across the myocardial vasculature during acute infarction. As noted earlier, there is a small incidence of hypotension with an inappropriate heart-rate response that responds to atropine. Other analgesic agents used for the treatment of pain include meperidine and pentazocine.
d. Beta-blockers— Beta-blockers are commonly used to treat the chest discomfort associated with AMI in countries outside the United States. They have been shown to be effective, apparently because of both their membrane-stabilizing effects and their beneficial effects on myocardial oxygen supply and demand. Small doses of metoprolol (generally 5 mg), propranolol (1–3 mg IV) or esmolol (a loading dose of 250 mg/kg followed by 25–50 mg/kg/min, up to a maximum dose of 300 mg/kg/min) can be given as long as hemodynamic and electrical stability can be maintained. Although esmolol's efficacy in this area is not well established, it is rapidly metabolized by esterases in red cells and is the only agent with a brief duration of action. Beta-blockers may also be useful in reducing the extent of infarction and for secondary prevention (see section d. Adjunctive therapy).
e. Angiotensin-converting enzyme inhibitors— Patients with ST elevation infarction seem to benefit from the early initiation of treatment with angiotensin-converting enzyme inhibitors (ACEI) if blood pressure allows. This strategy improves ventricular remodeling acutely but is even more efficacious over the longer term
4. Activity— Bed rest, except for the patients who require the use of a bedside commode, is mandatory during the first 24 h; autonomic instability, hypotension, and arrhythmias are common. It was believed in years past that strict bed rest was appropriate for 7–10 days and that discharge should occur after approximately 2 weeks. It is now clear that it is less stressful and thus more beneficial medically if hemodynamically stable patients are allowed to sit in a chair and use a bedside commode after 24 h. In general, patients without complications remain in an intensive care unit for 2–3 days, during which time their activities are markedly restricted. On transfer out of the intensive care unit, they can gradually begin ambulation, and most patients without complications can be discharged as early as 4 days after infarction.
5. Diet— It generally has been recommended that patients with acute infarction avoid extremes of hot and cold, have no caffeine, and be maintained initially on a liquid diet. The rationale for this approach includes the presence of autonomic instability, concerns that caffeine might exacerbate arrhythmias, and fear that particulate matter could be aspirated in the event of cardiac arrest (which tends to occur early during the evolution of acute infarction). Although none of these concerns have been strictly validated, such restrictions are considered prudent. After the first day, if patients are stable, their diet can be advanced. Education to facilitate good eating habits and a reduction in fat intake can be initiated at that time.
6. Bowel care— Patients, especially those who are older and are put to bed-rest with a reduced oral intake, have a tendency to constipation. Given the autonomic instability indigenous to AMI, the reduction of straining when bowel movements occur is recommended. In general, the use of stool softeners such as docusate sodium in a once-a-day dose of 100 mg is adequate. Some degree of selection is appropriate; some patients are not in need of this treatment, whereas others require more potent treatment.
7. Sedation— If patients are excessively restless and no physical cause can be determined, sedation with small doses of a sedative-hypnotic agent such as diazepam is recommended. During the initial 24 h, the dosage should be the minimum required to relieve anxiety, and patients should be continually reassessed to ensure that what is being treated is anxiety and not an underlying complication of infarction.
8. Electrocardiographic monitoring— All patients with significant likelihood of AMI should be monitored electrocardiographically. Those with chest pain and ECG changes that are highly likely to be due to infarction should be hospitalized in an intensive care unit. Those deemed at less risk still require ECG monitoring in an environment where defibrillation is readily available. It is recommended that patients with uncomplicated acute infarction be monitored until discharge; patients with complications require longer periods of observation.
9. Heparin— Unless there are contraindications to its use or patients are receiving other anticoagulants, all patients should receive subcutaneous heparin, 5000 units every 12 h. This regimen has been shown to reduce the incidence of deep venous thrombi that occurs in as many as 24% of treated patients; it should reduce the frequency of pulmonary emboli as well. Although the studies documenting these effects were done at a time when long periods of bed rest were mandated, they are most likely still correct—at least in principle—and there is little morbidity associated with the relatively modest doses of heparin. Therefore, despite earlier ambulation, the use of subcutaneous heparin twice daily is still recommended. Most patients with ST segment elevation AMI or with non-Q wave AMI benefit from the use of therapeutic doses of heparin. Many still recommend unfractionated heparin to increase the activated partial thromboplastin time (aPTT) to 1½–2½ times. However, it is now clear that LMWH is more beneficial in large part because its effects are consistent in most patients, with the exception of those with renal dysfunction. The usual dose is 1 mg/kg (enoxaparin q12h or 120 units IV/kg q12h for dalteparin. Monitoring of coagulation parameters is not necessary.

Ну и так далее. А вот лечение кардиогенного шока оттуда же:

[Dr.]

1. Ventilation-oxygenation— Because respiratory failure usually accompanies cardiogenic shock, every effort should be made to ensure adequate ventilation and oxygenation. Adequate oxygenation is essential to avoid hypoxia and further deterioration of oxygen delivery to tissues. The majority of patients with cardiogenic shock require mechanical ventilation with supplemental oxygen. Hypoventilation can lead to respiratory acidosis, which could exacerbate the metabolic acidosis caused by tissue hypoperfusion. Acidosis worsens cardiac function; it also makes the heart less responsive to inotropic agents.
2. Fluid resuscitation— Although hypovolemia is not the primary defect in cardiogenic shock, a number of patients may be relatively hypovolemic when shock develops following myocardial infarction. The causes of decreased intravascular volume include increased hydrostatic pressure and the increased permeability of blood vessels. Note that the physical examination may not always be helpful in determining the adequacy of left ventricular filling pressure. Furthermore, because the central venous pressure correlates poorly with PCWP in shock, it may not be useful, especially with a single reading. These facts underscore the importance of hemodynamic monitoring with a pulmonary artery catheter for an accurate assessment of left ventricular filling pressure. The optimal filling pressure is higher in patients with shock because the left ventricle is operating on a depressed function curve (less stroke volume for any given filling pressure). Generally, a PCWP of 18–22 mm Hg is considered adequate; further increases will lead to pulmonary congestion without a concomitant gain in cardiac output. Fluid resuscitation, when indicated by low or normal PCWPs, should be undertaken in boluses of 200–300 mL saline, followed by reassessment of hemodynamic parameters, especially cardiac output and PCWP.
3. Inotropic agents— A variety of drugs are available for intravenous administration to increase the contractility of the heart. Because the heart is operating on a markedly depressed Frank-Starling curve, a positive inotropic agent may improve the hemodynamic status significantly.
a. Digoxin— Although digoxin benefits patients with chronic congestive heart failure, it is of less benefit in cardiogenic shock because of its delayed onset of action and relatively mild potency (compared with other available agents).
b. Beta-adrenergic agonists— Dopamine is an endogenous catecholamine with qualitatively different effects at varying doses. At low doses (less than 4 µg/kg/ min) it predominantly stimulates dopaminergic receptors that dilate various arterial beds, the most important being the renal vasculature. Intermediate doses of 4–6 µg/kg/min cause b1-receptor stimulation and enhanced myocardial contractility. Further increases in dosage lead to prominent a-receptor stimulation (peripheral vasoconstriction) in addition to continued b1 stimulation. Dopamine improves cardiac output, and its combination of cardiac stimulation and peripheral vasoconstriction may be especially beneficial as initial treatment of hypotensive patients in cardiogenic shock.
Dobutamine is a synthetic sympathomimetic agent that differs from dopamine in two important ways: It does not cause renal vasodilation, and it has a much stronger b2 (arteriolar vasodilation) effect. The vasodilatory effect may be deleterious in the hypotensive patients because a further drop in blood pressure may occur. On the other hand, many patients with cardiogenic shock experience excessive vasoconstriction and inappropriately elevated afterload as a result of the natural sympathetic discharge or of treatment with inotropic agents, such as dopamine, that also have prominent vasoconstrictor effects. In such patients, the combination of cardiac stimulation and decreased afterload with dobutamine may improve cardiac output without a loss of arterial pressure.
Isoproterenol is also a synthetic sympathomimetic agent. It has very strong chronotropic and inotropic effects, resulting in a disproportionate increase in oxygen consumption and ischemia. It is therefore not generally recommended for cardiogenic shock except for bradyarrhythmias responsive to its chronotropic effect.
Norepinephrine has even stronger a and b1 effects than dopamine and may be beneficial when a patient continues to be hypotensive despite large doses of dopamine (more than 20 µg/kg/min). Because of the intense peripheral vasoconstriction that occurs, perfusion of other vascular beds such as the kidney, extremities, and mesentery may be compromised. Therefore, norepinephrine cannot be used for any extended time unless plans are made for definitive treatment. Beta-adrenergic agonists, which are extremely useful agents for improving the circulatory state of patients with cardiogenic shock, can also have adverse effects. Their ability to increase cardiac output is accompanied by an increased oxygen demand from enhanced contractility, a faster heart rate, and increased blood pressure—which can be harmful to the already ischemic myocardium. In addition, b-agonists can precipitate serious ventricular or atrial tachyarrhythmias.
c. Phosphodiesterase inhibitors— The intracellular mediator of b-adrenergic-receptor stimulation is cyclic adenosine monophosphate (cAMP), produced by adenylate cyclase after stimulation of the receptor. Cyclic-AMP in turn increases calcium influx into the cell, thereby increasing contractility. The phosphodiesterase inhibitors, such as milrinone and amrinone, inhibit the breakdown of cAMP by phosphodiesterase, prolonging its effect on cardiac contractility. These agents also act on cAMP produced at sites of b2 stimulation to prolong the vasodilatory effects. Phosphodiesterase inhibitors appear to have no advantage over the b-agonists in patients with cardiogenic shock.
4. Vasodilators— Vasodilation (especially of the arterioles to reduce afterload) is often necessary because of the increased levels of catecholamines and resultant peripheral vasoconstriction. Vasodilators are also useful in patients who require the enhanced contractility of b1 stimulation by an adrenergic agonist, even though the associated vasoconstriction (especially with dopamine) may inappropriately increase the afterload. In addition, the preload may be inappropriately high in many patients; here, a venodilator will be beneficial in reducing filling pressure (preload).
a. Nitroprusside— Nitroprusside is a direct-acting vascular smooth muscle relaxant, with a balanced effect (vasodilation of both the arterial and venous beds). It is commonly used in combination with an inotropic agent. Doses begin as low as 0.25–0.5 µg/kg/min and may go as high as 8–10 µg/kg/min. Even though nitroprusside is a very short-acting drug, hypotension is a common side effect, and close arterial pressure monitoring is required.
b. Phentolamine— Phentolamine is an a-antagonist that acts predominantly on arterial a receptors to produce vasodilation. It is not commonly used because of the tachycardia induced by the release of cardiac norepinephrine stores.
c. Nitroglycerin— Nitroglycerin is primarily a venodilator, although it may have some arterial effects at high doses. Its benefits arise from a decrease in pulmonary congestion and, through its coronary vasodilatory effects, a decrease in myocardial ischemia. It is not commonly used in cardiogenic shock, however, unless coronary vasospasm is thought to be contributing to myocardial ischemia.
5. Circulatory support devices— Among the mechanical devices developed to assist the left ventricle until more definitive therapy can be undertaken, the intraaortic balloon pump (IABP) has been in use the longest and is the most well studied.

[Dishifrator]

Сообщение от Algor

Уважаемые доктора!
Хотел бы проконсультироваться у кардиологов, как у узких специалистов, по поводу применения адреналина в острейшем периоде инфаркта миокарда. Вышел у меня недавно спор с анестезиологом по этому поводу, вот я и хочу разобраться. Как я понимаю, адреналин резко увеличивает потребность миокарда в кислороде, поэтому не может быть рекомендован даже при кардиогенном шоке?
Если не сложно, выскажитесь пожалуйста по этому поводу, желательно с ссылками, в т.ч. на англоязычные ресурсы. Хотелось бы услышать позицию по этому вопросу доказательной медицины. Также поделитесь собственным мнением, случаями из практики и т.д.

Ну это смотря с какой целью применять адреналин...
Разве только что при асистолии. Во всех других случаях при ОИМ его применять и вовсе не стОит. Да и с какой целью?

[Algor]

При асистолии только в рамках сердечно-легочно-мозговой реанимации. А просто при инфаркте? Вот и я о том же - смысл? АД дофамином поднимать нужно! И, наоборот, применять в-адреноблокаторы, чтобы уменьшить потребность сердечной мышцы в кислороде, а не миметик - адреналин, который резко эту потребность увеличивает. Спасибо Александру за содержательный ответ

[Straus]

Одновременное применение дофамина и бета-блоков - это вряд ли. Нынешнее место адреналина, мне кажется, в сердечно-легочной реанимации, и все. Коррекция АД при ОИМ - это вариации на тему норадреналин-дофамин-добутамин в зависимости от конкретной гемодинамической ситуации. Лучше, полагаю, в случае чего вспомогательное кровообращение, но, увы, это не в нашей жизни.
Для адреналина могу предложить еще одно место: в небулайзер, когда нет бета2-агонистов. Пробовал по бедности жизни.
...Ну, или если очень хотите спровоцировать аритмию , но это уже из арсенала гестапо.
Кстати, Algor, а конкретно какая была ситуация, что вызвала спор?

[beldmit]

При лечении КШ у больных острым ИМ используются три миметика:норадреналин,дофамин,добутамин.У каждого препарата есть свои достоинства и недостатки.
Норадреналин..Достоинства 1.наиболее сильный вазопрессор(можно использовать при АД 70 и ниже.2.Широкое терапевтическое окно 3-30 мкг/мин.
Недостатки:1.Резко нарушает перфузию тканей,вызывая лактатный ацидоз.2.Значительно повышает давление в легочной артерии,провоцируя отек легких.3.Быстрое развитие толерантности
Дофамин Достоинства1.в низких дозах увеличивает почечную перфузию.2.Наиболее популярный вазопрессор.Недостатки:1. "узкое терапевтическое окно-в дозах более 1000 мкг/мин. вызывает тахикардию,аритмии,провоцирует ангинозные боли.
Добутамин Достоинства:1.Единственный из вазопрессоров снижает давление в легочной артерии.Недостатки-слабый вазопрессор.
Адреналину место не нашлось,хотя после АКШ при развитии послеопрерационного шока кардиохирурги его иногда используют,т.к.при полной реваскуляризации не боятся синдрома "обкрадывания"иногда сочетают с дофамином,иногда используя сразу 3 прессора.
На самом деле,после исследования SHOCK-введение вазопрессоров при шоке-это устаревший паллиатив.Эти больные должнв "садиться "на контрпульс и подаваться в рентгеноперационную для проведения пластики нифарктсвязанного сосуда как можно быстрее,во всяком случае до 75 лет.
В Российских условиях обязательно введение в первые 6 часов тромболитиков(здесь лучше стрептокиназу,чем ТАП)

[Algor]

Сообщение от Straus

Кстати, Algor, а конкретно какая была ситуация, что вызвала спор?

Да банальная довольно...просто спор с одним анестезиологом, который утверждал, что применение адреналина оправданно при инфаркте миокарда на этапе скорой помощи, чтобы "дотянуть больного до госпиталя"

[alex_md]

Сообщение от beldmit

...здесь лучше стрептокиназу,чем ТАП

На основании каких данных сделан вывод о преимуществе киназы? Укажите пожалуйста источники.

[beldmit]

Уважаемый Alex.
В настоящее время было бы наивным на РКИ по сравнению стрептокиназы и ТАП в лечении КШ,поэтому приходится рассчитывать на здравый смысл.При низкой коронарной перфузии,сопровождающей КШ,системная активация плазмина окажет больший тромболитический эффект,чем использование селективного тромболитика

[Kosolapov]

Algor!
Опыт использования адреналина при ОИМ есть. Инфузия шла 4 – 7 мкг в минуту. Основанием для такого лечения служил опыт кардиохирургов. Применяли в период, когда с тромболитиками было совсем плохо. Приходилось наблюдать тяжеленные, торпидные кардиогенные шоки, когда больной уже получал большие дозы допамина (до 2 – 2,5 мг в минуту). Адреналин применялся «сверху». Утверждать, что это увеличивало выживаемость не могу, но продолжительность жизни (или агонии?) увеличивало. Создавалась иллюзия, что помогаем больному. (Общеизвестно, что кардиогенный шок лечат только контрпульс, а затем кардиохирургия). Количество аритмией не увеличивал. На мой взгляд, дофамин более аритмогенен. А потребность миокарда в кислороде как можно померить у конкретного больного? По ЧСС? Необъективно.
Применил бы адреналин сейчас? Наверное, только как Ваш оппонент, чтобы транспортировать больного. Например из ЦРБ до кардиохирургического центра.

[papadoctor]

Сообщение от beldmit

При лечении КШ у больных острым ИМ используются три миметика:норадреналин,дофамин,добутамин.У каждого препарата есть свои достоинства и недостатки.
Норадреналин..Достоинства 1.наиболее сильный вазопрессор(можно использовать при АД 70 и ниже.2.Широкое терапевтическое окно 3-30 мкг/мин.
Недостатки:1.Резко нарушает перфузию тканей,вызывая лактатный ацидоз.2.Значительно повышает давление в легочной артерии,провоцируя отек легких.3.Быстрое развитие толерантности
Дофамин Достоинства1.в низких дозах увеличивает почечную перфузию.2.Наиболее популярный вазопрессор.Недостатки:1. "узкое терапевтическое окно-в дозах более 1000 мкг/мин. вызывает тахикардию,аритмии,провоцирует ангинозные боли.
Добутамин Достоинства:1.Единственный из вазопрессоров снижает давление в легочной артерии.Недостатки-слабый вазопрессор.
Адреналину место не нашлось,хотя после АКШ при развитии послеопрерационного шока кардиохирурги его иногда используют,т.к.при полной реваскуляризации не боятся синдрома "обкрадывания"иногда сочетают с дофамином,иногда используя сразу 3 прессора.
На самом деле,после исследования SHOCK-введение вазопрессоров при шоке-это устаревший паллиатив.Эти больные должнв "садиться "на контрпульс и подаваться в рентгеноперационную для проведения пластики нифарктсвязанного сосуда как можно быстрее,во всяком случае до 75 лет.
В Российских условиях обязательно введение в первые 6 часов тромболитиков(здесь лучше стрептокиназу,чем ТАП)

А с каких пор Добутамин стал вазопрессором?

[beldmit]

Уважаемый papadoctor.Разумеется,Вы правы.Добутамин,будучи В1-миметиком ,никак не может быть вазопрессором.
Впрочем , Ваше замечание никак не влияет на суть обсуждаемой проблемы.

[beldmit]

Уважаемые коллеги.
Вероятно,это полный офф-топик,но меня интересует проведение тромболизиса на фоне предшествующей терапии непрямыми антикоагулянтами.
1.Проводим тромболизис ,не определяя МНО или задерживаем проведение тромболизиса,определяя МНО?
2.Если МНО более 3,будем проводить тромболизис?Есди будем,то чем(стрептокиназа,ТАП)?Будет ли в этом случае проводиться адъювантная терапия(НФГ,низкомолекулярные гепарины)?