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#1
08.05.2005, 11:38
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ФЖ и адреналин
Здравствуйте! Хотелось бы знать Ваше мнение, коллеги: дело в том, что у нас разгорелся спор по поводу применения адреналина для купирования приступов фибрилляции желудочков. Знаю, звучит скверно, но суть именно к этому и сводиться. Позиция моих оппонентов такова: вот он перед нами больной с ФЖ, зарегестрированной на мониторе дефибриллятора. После проведения 3 - х кратной эл. дефибрилляции (неуспешно, допустим) они рекомендуют вводить адреналин и лишь спустя полминуты - минуту кордарон. Вот этого я понять и не могу: зачем? Ладно бы кто - нибудь был на моей стороне, может мы и доказали бы что - либо, однако, один в поле не воин.
 На мою просьбу объяснить для чего он нужен мне объяснили буквально следующее: "Ну как же, для того, чтобы сжать артериолы". Тут я совсем раскис...Коллеги, может кто - нибудь подскажет, где они это вычитали. Буду очень признателен. С уважением, Дмитрий. ЗЫ: а может он и правда нужен?.. 
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#2
08.05.2005, 13:29
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Уважаемый коллега!
Похоже, что Ваши коллеги правы (по крайней мере, согласно гайдлайну): American Heart Association in collaboration with the International Liaision Committee on Resuscitation (ILCOR). International Guidelines 2000 for Cardiopulmonary resuscitation and Emergency Cardiovascular Care A consensus on Science. European Resuscitation Council. Resuscitation 2000; 46: 103252. Вот фрагмент недавней статьи от финских коллег (описание протокола): The Helsinki EMS implemented the Resuscitation 2000 guidelines into the CA treatment protocol in October 2000. The main difference from the former treatment protocol was that amiodarone replaced metoprolol as the antiarrhythmic adjunct in resuscitation. Accordingly, after three ineffective shocks, one sequence of cardiopulmonary resuscitation (CPR), administration of 1 mg of adrenaline (epinephrine), a bolus of 300 mg of amiodarone (Cordarone® Sanofi-Synthelabo, SPSS, Espoo, Finland) was administered. Differently from previous studies and Guidelines, аmiodarone (50 mg/ml) was administered without dilution as a bolus into a vein located as centrally as possible (external jugular or antecubital vein). This was performed to save time because the dilution process in 5% glucose was found to take approximately 90 s. To reduce the hypotensive effects of amiodarone, a rapid bolus of approximately 200 ml of acetated Ringer's solution was given. The amount of fluid bolus was chosen because CAs with VF or ventricular tachycardia (VT) are seldom associated with hypovolemia and, in accordance with the guidelines, the patient had already received adrenaline, a vasopressor. If the heart was still in VF after three sequences of CPR, an additional dose of 150 mg of amiodarone was administered. The same treatment protocol applies if in patients with asystole or pulseless electrical activity (PEA) as the initial rhythm, VF develops during resuscitation. Blood pressure is measured immediately after achieved return of spontaneous circulation (ROSC) and thereafter every 5 min, using non-invasive oscillotonometry. Из Acta Anaesthesiol Scand. 2004 May;48(5):582-7. The use of undiluted amiodarone in the management of out-of-hospital cardiac arrest. Skrifvars MB, Kuisma M, Boyd J, Maatta T, Repo J, Rosenberg PH, Castren M. Не в тему, но намой взгляд интересная статья о сравнении адреналина и вазопрессина при серд. реанимации: Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH; European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study Group. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004 Jan 8;350(2):105-13. [Ссылки доступны только зарегистрированным пользователям ]
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#3
08.05.2005, 14:05
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Дополнение: фрагмент публикации о консенсусе 2000 (будет интересен полный текст вышлю ПДФ)
New Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care Changes in the Management of Cardiac Arrest Karl B. Kern, MD; Henry R. Halperin, MD; John Field, MD JAMA. 2001;285:1267-1269. Pharmacology of ACLS Perhaps the most controversial recommendations in the ACLS portion of the new Guidelines concern the addition of vasopressin and amiodarone in the algorithm for ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest. In past CPR guidelines, epinephrine has been recommended if spontaneous circulation is not restored following 3 defibrillating shocks. Experimental animal data supporting the use of epinephrine are convincing. The primary benefit of epinephrine during CPR is to increase peripheral vasoconstriction. This results in increased perfusion pressures, increased myocardial and cerebral blood flow, and improved outcome. However, the data for clinical cardiac arrest are much less definitive. No adequate trial of epinephrine vs placebo has ever been completed in humans. Clinical trials of standard vs high-dose epinephrine have been completed, but none used a placebo control. Recently, interest in vasoconstrictors other than epinephrine has led to both experimental and some preliminary clinical trials with vasopressin. The data are thus far remarkably homogeneous. Animal studies have almost always (21/23 studies at the time of the Guidelines review) supported improved hemodynamics, myocardial blood flow, and short-term outcome with vasopressin vs either placebo or epinephrine. A small pilot study (n = 40) that randomized patients in refractory cardiac arrest to either vasopressin (40 U intravenously) or epinephrine (1 mg intravenously) found improved 24-hour survival, but no difference at hospital discharge, with vasopressin.18 No difference in outcome was found in an unpublished study reviewed during the deliberations of a 200-patient, in-hospital trial of vasopressin vs epinephrine (Ian Stiell, MD, MSc, unpublished data, 2000). No clinical data yet exist for vasopressin vs placebo in human cardiac arrest. The conference conclusion was that vasopressin is an effective vasoconstrictor and can be used once as an alternative to epinephrine for the treatment of shock-refractory ventricular fibrillation (IIb). Repeated efforts to show efficacy for antiarrhythmics administered during CPR for shock-refractory ventricular fibrillation have failed until recently. Amiodarone was recently found to improve survival to hospital admission in the Amiodarone for Resuscitation After Out-of-Hospital Cardiac Arrest Due to Ventricular Fibrillation (ARREST) trial, a prospective, randomized, double-blind, placebo-controlled clinical trial of amiodarone during CPR in patients with out-of-hospital cardiac arrest due to shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.19 Importantly, amiodarone was not compared with lidocaine or other antiarrhythmic drugs in this trial. A total of 504 patients who experienced out-of-hospital cardiac arrest were enrolled. Each patient was in ventricular fibrillation despite at least 3 defibrillation shocks, had already been intubated, had intravenous access, and had received 1 mg of epinephrine. The primary end point of survival to hospital admission was significantly better in the amiodarone group compared with placebo group (108/246 [44%] vs 89/258 [35%]; P<.03). Though this surrogate end point was recognized by the Guidelines participants not to be the final answer, the trial marked the first time any improvement with antiarrhythmic therapy administered during cardiac arrest had been found. Noteworthy was the interval to treatment. The mean (SD) interval from telephone call to drug administration in the amiodarone group was 21 (8) minutes. There is hope that even more powerful outcome improvements may be possible if the drug can be administered earlier. Caution is warranted however until more data are available. For example, some vasoconstrictive agent may be necessary during CPR before administering amiodarone to counteract its potent vasodilatory properties. Based on the ARREST trial, amiodarone was recommended for consideration as an alternative to lidocaine in shock-refractory ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest (IIb). Lidocaine remains an alternative choice but since it has little outcome data supporting its use it received only an indeterminate recommendation. Bretylium tosylate was eliminated from the algorithm because of a lack of demonstrated efficacy and because it is no longer being produced. Сам консенсус располагается на [Ссылки доступны только зарегистрированным пользователям ]
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#4
08.05.2005, 15:16
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Цитата:
[Ссылки доступны только зарегистрированным пользователям ]
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#5
09.05.2005, 14:09
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Уважаемый Dishifrator.
Адреналин при ФЖ вводится не для того,чтобы купировать ФЖ,а для того.чтобы повысить чувствительность ФЖ к последующим эл.импульсным разрядам.Повышая возбудимость миокарда,адреналин может перевести мелковолнорвую ФЖ в крупноволновую.Немаловажную роль играет и повышение коронарного кровотока,как за счет вазопрессорного ээфекта,так и за счет расширения коронарных артерий.
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#6
09.05.2005, 17:49
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Цитата:
, однако, речь идет как бы о крупноволновой фибрилляции. Т.е. если не разделять ФЖ на крупно - и мелковолновую а принять ее, как единую. Еще вот на счет вазопрессорного эффекта адреналина немного сомневаюсь - для этой цели не самый лучший препарат. ЗЫ: В вопросе разобрались. Дискуссию пытаюсь продолжить исключительно ради развития темы. ЗЫЫ: ОГРОМНОЕ СПАСИБО Вадиму Валерьевичу за статьи!
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#8
10.05.2005, 19:46
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Так эта схема, как мне кажется, не есть секрет Полишинеля, вот например товарищи с фельдшер.ру давно прибрали к рукам [Ссылки доступны только зарегистрированным пользователям ]. Весит полтора мегабайта где-то, бесплатно, конечно
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Линейный вид
