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#61
24.04.2006, 21:49
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ЭКГ месяца
Потрясающий случай, представленный на www.acc.org!
Увы, но ресурс сейчас платный и не всем доступен. Очень подходит под определение пароксизмальной тахикардии. Надеюсь, мне простят не соблюдение копирайтов  "Представленная ЭКГ записана у пациента в БИТе. Пульс - 70, АД - 110/60, ЧДД - 18. ОН бодрствует, жив (alert), сидит в кровати и кушает свой ланч. 1. Как такое возможно? 2. Не артефакт ли на ЭКГ?" Продолжение завтра 
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#63
24.04.2006, 22:25
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Интересно, а пульс 70 прямо во время этой записи? Если нет, то можно предположить, что это неустойчивый пароксизм ЖТ, случайно попавший на ЭКГ. Я такое видел у больного с ДКМП: по монитору идет вот такая же гадость в течение около 10 с, а больной спокойно мажет бутерброд.
Еще возможный вариант -- больной на АИК или с искусственным левым желудочком.
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#65
25.04.2006, 08:59
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Цитата:
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#68
25.04.2006, 22:09
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Продолжение..
"Взгляните на ЭКГ ещё раз. Это может быть и фибрилляция желудочков, и артефакт, так как ФЖ гемодинамически нестабильное (неперфузируемое) нарушение ритма. НО ЭТО ФИБРИЛЛЯЦИЯ ЖЕЛУДОЧКОВ (кроме шуток, прим. переводчика ). При каких условиях это возможно? Почему пациент гемодинамически стабилен? (и ест ланч, гад!! Прим. переводчика)"
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#69
25.04.2006, 22:11
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Правильный ответ:
"Since VF and hemodynamic stability are mutually exclusive, there must be a trick. This patient had a left ventricular assist device (LVAD) implanted as a bridge to cardiac transplant. LVADs are typically not gated to the QRS complex, and pump independently of the cardiac rhythm. Thus ventricular tachycardia, and even ventricular fibrillation have little impact initially on systemic blood pressure output in these patients; device flow does decrease with VT or VF. The risk of thromboembolic complications may increase. With sustained VT or VF, however, these patients can develop right heart failure, since the LVAD only supports the left ventricle. During VF in a patient with an LVAD, the right ventricle does not contract, and acts as a passive conduit between the right atrium and pulmonary artery. For this reason, sustained VT or VF should be treated, and patients with recurrent VT or VF should be treated with antiarrhythmic drugs in efforts to suppress the arrhythmia. Rarely, a right ventricular assist device may be needed in patients with intractable ventricular arrhythmias. Intravenous amiodarone did not terminate the VF. The patient was sedated and defibrillated. Reference Oz MC, et al. Malignant ventricular arrhythmias are well tolerated in patients receiving long-term left ventricular assist devices. J Am Coll Cardiol 1994; 24: 1688-91."
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#70
25.04.2006, 22:14
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Бонус: очень интересная дискуссия по поводу ЭКГ месяца с ответами на ряд интересных вопросов.
"Respond to ECG of the month Dr. Ganz of the ACC is available to answer questions pertaining to the ECG of the Month series. Read what others have asked and take the opportunity to participate. Post a Response Posting submitted by: Hisham Maher Selim sent on: 07/06/02 Excellent Case as usual. My question is, from the case history the patient was in severe cardiomyopathy, for how long the LVAD, could be working well , and what will be the situation in case for any reason the donor heart is not available? Thanks. Hisham Selim, Egypt Dr. Ganz: In this patient, the LVAD was placed as a "bridge" to cardiac transplant. In this setting, LVAD support may be prolonged. In the recently published REMATCH trial, LVADs were used to support patients who were not transplant candidates. In this trial, the median survival in the LVAD patients was 408 days. I suspect that as LVAD technology improves, more patients will receive this treatment modality, for longer and longer periods of time. Posting submitted by: Wenyi Yang sent on: 06/24/02 When is the patient indicated for heart transplanatation? What is the indication for chronically anticoagulate the patient with LVAD? Or was he already on warfarin? Dr. Ganz: The patient was on the transplant list prior to LVAD insertion , but then decompensated, requiring mechanical assistance. Because of the type of LVAD that was implanted, he was started on warfarin. Posting submitted by: Roy Avalos, Sen Ji sent on: 06/19/02 Dr. Ganz: It's a very interesting case. RV VF is a possibility. Our question is why we do not see any LV electrical activity. Thanks. Regards, Roy and Sen Dr. Ganz: Even though the mechanical function of the heart is managed by the LVAD, normal electrical activation continues. Thus, patients with LVADs (or BiVADs) can have sinus rhythm, atrial fibrillation, or in the cases posted, ventricular fibrillation or ventricular tachycardia. In general, LV electrical activation dominates over RV activation in the surface ECG, because of the larger muscle mass in the LV. Posting submitted by: dr.subhashtelang sent on: 06/16/02 i have never seen a pateint of VF sitting & having lunchin my clinical practice of 19yrs.ECELLENT ECG. DR SUBHASH TELANG Dr. Ganz: It doesn't happen very often....Thanks very much for the comment. Posting submitted by: Atul Khasnis sent on: 06/08/02 This appears to be a relatively sustained episode of ventricular fibrillation. Even in the presence of a LVAD, if the right ventricle is fibrillating (the output is virtually zero), what maintains the cardiac output of the LV(and hence the blood pressure) in these patients? Why was amiodarone chosen as a first option in this case? Dr. Ganz: The concept of the RV as a passive conduit is not new; the Fontan procedure completely bypasses the RV (caval-pulmonary artery anastomosis) in patients with tricuspid atresia. Amiodarone was chosen probably because of the frequency with which it is used in severe cardiomyopathy; given the assist device,however, other agents could very well have ben chosen. Posting submitted by: Luca Mascitelli sent on: 06/07/02 A beautiful case, as usual! I think that the presence of an artifact was unlikely because portions of QRS complexes at the sinus-cycle length were not visible within the ecg! L.M. Italy Dr. Ganz: Exactly right! WIth artifact, you can usually pick out something resembling a QRS complex marching through in one (or more) of the leads. Posting submitted by: Dr.A.G.Deketele sent on: 06/05/02 Does this patient have a tremor? Dr. Ganz: No, though artifact due to a tremor is a good thought. With tremor, though, the QRS complexes are usual apparent despite the baseline artifact. Posting submitted by: M.Smith sent on: 06/04/02 How long does it take the RV to fail, minutes, hours, days? Thanks. Dr. Ganz: That is a good question; it probably varies tremendously by patient. In the original series reported by Oz et al, episodes ranged in duration from 15 minutes to 12 days. Last week I cardioverted a patient with BiVADs who had been in ventricular tachycardia/flutter at 302 bpm for at least 5 days. He was hemodynamically stable, but felt mildly lightheaded and short of breath. Posting submitted by: Michael A. Shapiro, MD sent on: 06/04/02 These cases have become quite common in institutions with a busy VAD program, but the first time you have a conversation with a patient in VF, it's a bit disconcerting. I have seen patients in whom conversion from an LVAD to BiVAD was needed only because of arrythmia-induced RV standstill. Dr. Ganz: This has been my experience as well. And I agree, sustained, hemodynamically tolerated VF is hard to get used to..."
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#71
04.05.2006, 21:55
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Очередная тахикардия. Пароксизмальная.
1. Холтер. Синусовый ритм.
2. Желудочковая экстрасистола. 3-4. Пароксизмальная тахикардия Во время пароксизма пациентка 72 лет жалуется на сердцебиение, АД 132/70 Hg, в сознании. Тактика: 1. Экстренная кардиоверсия 2. Плановая кардиоверсия 3. Новокаинамид в/в 4. Б-АБ 5. Дигоксин 6. Лидокаин 7. Верапамил
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#72
05.05.2006, 16:17
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Продолжительность пароксизмов какова? Может они спонтанно купируются?
Тем более гемодинамика стабильна. И еще, базовый ритм до такой частоты как разгоняется? Скачком?IMHO: впечатление трепетания предсердий 2:1, с аберрацией. В третьем файле холтера базовый ритм, похоже, трепетание без аберрации, частота ближе к 140, во втором отведении "псевдо R-штрих" виден...) Пациентка вообще, какую-нибудь терапию получает?
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#73
05.05.2006, 17:21
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Думаю, что это ФП/ТП с аберрацией (RR разные, там где аберрация). Насчет кардиоверсии (не экстренной) - не знаю, (судя по ЭКГ с синусом, там предсердия большие), а так можно БАБ+дигоксин.
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#74
05.05.2006, 19:21
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на первый взгляд похоже на VT. особенно "тахиикардия2", где узкий комплекс смахивает на синусовый захват. А вот по поводу ЖЭС, есть сомнения, не AV-узловая ли аберрантная? там на ST-сегменте что-то похожее на ретроградный P. Хотя м.б. и желудочковая.
По-поводу ТП - тоже не исключается там где "тахикардия" во 2-м участке с узкими комплексами проглядывется что-то напоминающее волны трепетания... я бы дал кордарон
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#75
17.05.2006, 21:54
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Прошу прощения за отсутствие. Удалось посетить между праздниками славный город Минск.
На представленной ЭКГ - аберрация на мерцании. Дифф. диагноз с ЖТ. 1. При тахикардии с широкими комплексами и стабильной гемодинамике препарат выбора новокаинамид или соталол. Амиодарон эффективнее при снижении фракции выброса и сердечной недостаточности. (ACC/AHA/ESC guidelines for the management of patients with SVA). 2. При аберрации на мерцании возникают мысли о WPW. A rapid, irregular, sustained, wide-QRS-complex tachycardia strongly suggests AF with conduction over an accessory pathway or AF with underlying bundle-branch block. Extremely rapid rates (over 200 bpm) suggest the presence of an accessory pathway. Иногда (скрытый WPW) даже приходится делать ЭФИ. Electrophysiological studies may be helpful when sinus node dysfunction is suspected and to clarify the mechanism of wide QRS complexes during AF. В связи с этим, верапамил/дилтиазем, дигоксин противопоказаны. Б-АБ, скроее всего, будут неэффективны. Ну и без новокаинамида, видимо, никуда.. У нас, кстати, появился феррейновский (аритмологи плюются..)новокаинамид. When a patient with a preexcited tachycardia is clinically stable, intravenous procainamide may be given to convert the atrial mechanism to sinus rhythm. It is critically important to avoid agents with the potential to increase the refractoriness of the AV node, which could encourage preferential conduction over the accessory pathway. Specifically, administration of AV nodal blocking agents such as digoxin, diltiazem, or verapamil is contraindicated. Beta-blockers are ineffective in this situation, and their administration by the intravenous route may have adverse hemodynamic effects. Intravenous adenosine may be used when the QRS complex is narrow (less than 120 ms duration) during the tachycardia, because this indicates that antegrade conduction is occurring through the AV node (ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation).
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Линейный вид
