[LupusDoc]

Заранее приношу извинения по поводу скудности информации. По мере ее поступления постараюсь обновлять.
ЭКГ мужчины 76 лет, который выписан накануне из стационара после установки ЭКС (модель и режим пока уточнить не удалось). Причина установки ЭКС - преходящая полная АВ-блокада в сочетании с СССУ.
Сейчас жалобы на слабость, неопределенные боли за грудиной. Данных анамнеза нет (постараюсь по мере возможности уточнить).

Основной вопрос - о функционировании ЭКС.

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[Rodionov]

Для ответа на вопрос "работает-не работает", надо знать режим стимуляции.

На этой пленке частота сердечных сокращений около 75 в мин.
Если у него стоит однокамерный стимулятор в режиме желудочковой стимуляции (VVI), то вполне возможно, что в этой ситуации он просто "молчит".

Если стимулятор двухкамерный (что было бы логично при полной АВ-блокаде), тогда это непорядок.

Базовый ритм тут похож на узловой (Р позади комплекса QRS).

[tourunov]

УИР с ретроградным проведением на предсердия. Нужна карточка с данными на стимулятор (выдают при имплантации).

[azrev]

Прошу прощения.
На ЭКГ представлена эффективная стимуляция в режиме VVI с ЧСС 70 с ретроградным проведением на предсердия.

Красными точками обозначены спайки стимулятора:
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[Gilarov]

VVI, ретроградное проведение. Возможно развитие синдрома ЭКС (слабость, боли). Режим - не оптимальный. Скорее всего, нужно было DDD.

[Tim Hunter]

Да, мне тоже кажется, что ЭКС работает. Чтобы это было лучше видно, надо отключить фильтры на электрокардиографе, они просто срезают низкоамплитудные высокочастотные спайки.
Еще можно поднести магнит, если частота изменится, это тоже укажет на нормальную работу ЭКС.

[FRSM]

Со своей колокольни. Провели бы снимки гр. клетки (прямой и левый боковой), проследив все компоненты електродов.....

[Susanin]

Увы, там не будет видно, работает ли стимулятор
Зато там будет видно количество проводов и где они находятся.
Ведь логично при СССУ и АВ-блокаде поставить DDD(по возможности R).
Если провод на снимке один, значит как поставили, так и работает.
Если провода два, значит предсердный не работает. Может он не в предсердии вовсе, а может поломался.
Дешево и сердито.

[FRSM]

"Гиларов одобрил(а): Увы, там не будет видно, работает ли стимулятор..."

Многое можно увидеть.....Особенно, если имеются контрольные снимки после имплантации.

[Gilarov]

А что там можно увидеть, кроме дислокации или поломки электродов? Марку и модель стимулятора по его очертаниям?

[FRSM]

В частности:

Most pacemaker generators have an x-ray code that can be seen on a chest radiograph.

The markings, along with the shape of the generator, may assist with deciphering the manufacturer of the generator and pacemaker battery.

[FRSM]

Случай: [Ссылки могут видеть только зарегистрированные и активированные пользователи]

[FRSM]

Может быть, кому-нибудь будет интересным:

Pacemaker Syndrome and Pacemaker Complications


Synonym: AV dyssynchrony syndrome

This article deals with the complications of pacemakers, including pacemaker syndrome. Pacemakers are discussed further in the separate articles Pacemakers and Pacing, Inserting Temporary Pacemakers, and Implantable Cardioverter Defibrillators.

Pacemakers sense intrinsic cardiac activity and pacing is inhibited when this occurs:.
•Atrial pacing is used in sick sinus syndrome and in patients without any conduction disturbance.
•Ventricular pacing (pacing catheter in the right ventricle) is necessary for complete heart block.
.
Complications of permanent pacing1
Causes of pacing system malfunction include undersensing, oversensing, loss of capture, loss of output, inappropriate rate, inappropriate lead position, inappropriate mode, extracardiac stimulation, true pulse generator failure, pacemaker-mediated tachycardia (in dual-chamber pacemakers with DDD, VDD, and DDDR modes), pacemaker syndrome and inappropriate fiddling of the pulse generator by the patient. Most pacing system malfunctions are benign, but some can be life-threatening..
•Complications related to venous access include pneumothorax, haemothorax, and air embolism.
•Lead-related complications include perforation, dislodgment, diaphragmatic stimulation, and malposition (including passage into the left side of the heart via a septal defect). Cardiac tamponade, usually due to chamber perforation, should be suspected whenever hypotension occurs.
•Local pocket-related complications include haematoma, wound pain, pocket erosion, and infection.
•Pacemaker infection ranges from mild local pain and erythema to life-threatening septicaemia. The most common pathogens are coagulase-negative staphylococci, Staphylococcus aureus Gram-negative enteric bacilli and mixed infections.
•Delayed complications of permanent pacing leads include venous thrombosis, exit block, insulation failure, and conductor fracture. Late lead damage may be reduced by use of axillary or cephalic venous access.
•Most modern pulse generators have an expected longevity of 5-9 years and unexpected pulse generator (electrical) failure is rare.
•Lead-related problems (increased thresholds, decreased impedance) resulting in increased current drain are the most common causes of premature battery depletion.
•Lithium-iodine batteries used in current pulse generators are not rechargeable and surgical replacement of the entire generator is required.
.
Complications of temporary pacing2•Immediate complications include:◦Ventricular tachycardia or fibrillation
◦Arterial puncture
◦Pneumothorax
◦Brachial plexus injury

•Late complications include:◦Ventricular arrhythmias
◦Septicaemia (especially staphylococcal infection)
◦Wrong position requiring repositioning

.
Epidemiology•The rate of acute complications of pacemaker insertion is 4-5% and mostly related to operator experience.1
•The incidence of late complications of permanent pacemakers has been reported as 2.7%.1
.
Investigations3•Investigation for possible underlying myocardial infarction, including troponins and creatine kinase (which is elevated in myocardial injury and cardiac trauma).
•Coagulation screen: prevent bleeding complications during invasive procedures.
•Electrolytes: exclude electrolyte abnormalities that may affect pacing thresholds.
•Drug levels: e.g. digoxin and other antiarrhythmics that may alter pacing thresholds.
•Chest x-ray: evaluate lead position and fracture. A chest x-ray can be used to identify the pacemaker model, as most pacemakers have an x-ray code which is visible on a standard chest xray.
•Echocardiogram: to assess for inappropriate lead position, pericardia effusion or tamponade, or lead fracture.
•Pacemaker assessment:◦Evaluation of thresholds, lead impedance, and battery voltage, as well as review of histograms, mode switch episodes, and stored electrocardiograms.

•Magnet application:◦After magnet application, the pacemaker goes to asynchronous pacing mode at a programmed rate, which is unique to that model. This is helpful in diagnosis of loss of capture and battery depletion.

•ECG:◦To diagnose arrhythmias and also undersensing, oversensing, and capture loss.
◦The best method of diagnosis is to correlate symptoms with cardiac rhythms, e.g. using Holter monitoring and event recorders.

•Telemetry monitoring:◦Early recognition of loss of sensing and capture from lead dislodgement in immediate post-implant period.

•Transtelephonic monitoring:◦Early recognition of battery depletion based on the magnet rate, which is unique to each pacemaker model.

•Fluoroscopy:◦To evaluate lead fracture, especially during provocative manoeuvres.

.
Pacemaker syndrome
Pacemaker syndrome refers to the occurrence of symptoms relating to the loss of atrioventricular (AV) synchrony in patients with a pacemaker..
•Ventricular pacing has been shown to sacrifice the atrial contribution to ventricular output.
•In some cases, atrial contraction occurs against closed AV valves, producing reverse blood flow.
•In response to decreased cardiac output, total peripheral resistance is usually increased in order to maintain blood pressure but does not increase in some patients, resulting in decreased blood pressure.
•This combination of decreased cardiac output with a loss of the usual compensatory increase in total peripheral resistance contributes to the development of pacemaker syndrome.
•The incidence of pacemaker syndrome has been estimated to range from 7% (symptoms severe enough to warrant pacemaker revision) to 20% (mild to moderately severe symptoms).4 Asymptomatic pacemaker syndrome is probably common and the true incidence of pacemaker syndrome much higher.1
•In 1994 Furman redefined pacemaker syndrome as:5◦Loss of AV synchrony
◦Retrograde ventriculoatrial (VA) conduction
◦Absence of rate response to physiological need


Most authorities now understand pacemaker syndrome as being related to nonphysiological timing of atrial and ventricular contractions, which may occur in a variety of pacing modes. It has been proposed that pacemaker syndrome should be renamed as AV dyssynchrony syndrome, which better reflects the mechanism responsible for causing symptoms.6.
.

Risk factors6
•Patients with sick sinus syndrome frequently have preserved AV conduction.
•As many as 90% of patients with preserved AV conduction may have VA conduction, which predisposes them to pacemaker syndrome.
•Patients may have intact VA conduction not apparent at the time of implantation or may develop VA conduction at any time after pacemaker implantation.
•Patients with noncompliant ventricles and diastolic dysfunction (e.g. the elderly and patients with cardiomyopathy) are particularly sensitive to loss of the atrial contribution to ventricular filling.
.

Prevention
•Most cases of pacemaker syndrome occur with ventricular pacing and so atrial pacing should be used whenever possible.
•Alternatively, a dual-chamber system can be programmed to a long AV interval to promote intrinsic conduction, as long as dyssynchrony related to marked first-degree AV block is not present.
•Pacing parameters must be optimised, e.g. AV delay, to achieve physiological timing of atrial and ventricular contractions.
.

Presentation of pacemaker syndrome6
•The most common symptoms include pulsation and fullness in the neck, dizziness, palpitations, fatigue, light-headedness and syncope.
•Symptoms of heart failure may occur.1
•Symptoms can vary considerably and also vary in severity.
•Signs are also variable and include hypotension, tachycardia, tachypnoea, raised JVP and cannon waves.
•There may be variations in pulses and fluctuating blood pressure.
•A drop of 20 mm Hg or more during ventricular pacing compared with that during atrial or AV synchronous pacing is suggestive of pacemaker syndrome.
•Basal lung crepitations, tender and pulsatile liver and peripheral oedema may occur.
•Examination of the heart may demonstrate regurgitant murmurs and variability of heart sounds.
.

Differential diagnosis
•AV dyssynchrony may also occur without a pacemaker (called 'pseudopacemaker syndrome'), e.g. extremely prolonged first-degree AV block, nodal rhythm more rapid than the atrial rate (such as in children with sinus node dysfunction after congenital defect repair) and hypertrophic cardiomyopathy with complete AV block.6
•Possible other causes for the patient's presentation are pacemaker malfunction, inappropriate mode switching, worsening heart failure, recent change in medications (especially antihypertensives), paroxysmal atrial fibrillation, sinus tachycardia, autonomic dysfunction and respiratory tract infection.
.

Management
•In patients with other pacing modes, symptoms usually resolve after upgrading the pacemaker to a dual-chamber pacing system,7 or reprogramming the pacemaker parameters, e.g. atrioventricular (AV) delay, post-ventricular atrial refractory period, sensing level, and pacing threshold voltage.
•Medical therapy has a limited role but electrolyte abnormalities may need to be corrected and the medication regime should be reviewed and adjusted as needed.

[LupusDoc]

Большое спасибо, всем откликнувшимся в теме.

Согласно известной русской пословице, обещанного долгонько приходится ждать, информация о пациенте мне поступает весьма скупым ручейком... Сегодня вот удалось узнать, что модель ЭКС - Esprit SR однокамерный, на рентгене электрод в правом желудочке, так что видимо работает ЭКС так как ему и положено, другой вопрос - хорошо ли это для пациента... Да, еще из лекарственной терапии пациент сейчас принимает соталол 160 мг/сут (2 раза по 80 мг) и бисопролол 2,5 мг сут.

[audovichenko]

Как пить дать, синдром ЭКС :(... Можно попытаться включить сенсор для частотной адаптации, но есть риск, что этого все равно будет недостаточно и придется-таки повторно оперировать (имплантировать DDD).

[Gilarov]

Соталол+бисопролол - диковатая комбинация

[Susanin]

Бета-блокаторы + СССУ + ЭКС - можете пояснить зачем? Я не понимаю...
Частотная адаптация врядли что-то даст, скорее наоборот - при тахикардии еще хуже будет наполнение желудочков.
Показан DDDR

[Yariko]

не применительно к данному пациенту, просто, в поддержание разговора на тему ЭКС и бета-блокаторы. В исследовании DAPHNE изучали пациентов с фибрилляцией предсердий и с установленным двухкамерным водителем ритма по поводу синдрома слабости синусового узла на фоне терапии бета-блокаторами по сравнению с соталолом

The Drug And Pace Health cliNical Evaluation (DAPHNEstudy: A randomized trial comparing sotalol versus β-blockers to treat symptomatic atrial fibrillation in patients with brady-tachycardia syndrome implanted with an antitachycardia pacemaker
Background Atrial tachyarrhythmias (ATAs) are mainly treated by pharmacologic therapy for rate control or rhythm control. The aim of our study was to compare sotalol (S) versus β-blocking agents (BB) in terms of prevention of ATA, cardioversions (CVs), and cardiovascular hospitalizations (H) in patients paced for bradycardia-tachycardia form of sinus node disease (BT-SND).
Methods One hundred thirty-five patients (67 males, aged 73 ± 7 years) were enrolled in a prospective, parallel, randomized, single-blind, multicenter study. All patients received a dual chamber rate adaptive pacemaker; after 1 month, 66 patients were randomly assigned to BB (62 ± 26 and 104 ± 47 mg/d for atenolol and metoprolol, respectively) and 69 patients to S (167 ± 66 mg/d).
Results After an observation period of 12 months, the percentage of patients free from ATA recurrences was 29% in both BB and S group. Cardioversion and H were significantly (P b .01) fewer in the 12 months after implantation than in the 12 months before both in patients treated with S (CV 69.4% vs 22.2%, H 91.7% vs 33.3%) and in patients treated with BB (CV 58.5% vs 17.1%, H 82.9% vs 26.8%). Kaplan-Meier survival analysis showed a nonsignificant trend toward a lower incidence of the composite end point (CV + H) among BB patients.
Conclusions In the complex context of “hybrid therapy” in patients with BT-SND implanted with a modern dual chamber rate adaptive pacemaker device delivering atrial antitachycardia pacing, no differences were found between the use of β-blocker and the use of S, at the relatively low dose achieved after clinical titration, in terms of prevention of cardiovascular H or need for atrial CV. (Am Heart J 2008;156:373.e1-373.e8.)
Еще есть симпатичная статья Beta-blocker induced bradycardia—should we pace? на тему необходима ли установка кардиостимулятора пациентам с сердечной недостаточностью при невозможности назначения бета-блокаторов или их титрации до полной дозы

The European Journal of Heart Failure 6 (2004) 449–451

- Patients who tolerate a minimal beta-blocker dose should be up-titrated guided by the individual patient’s tolerability and heart rate response. These patients should not be paced to achieve a higher beta-blocker dose.
– In patients not tolerating a minimal beta-blocker dose due to sinus node dysfunction, atrial pacing (i.e. AAI) might be considered in individual patients to initiate a beta-blocker therapy.
– Although development of significant AV block with the use of a beta-blocker suggests that there is disease of the conduction system, in patients not tolerating a minimal beta-blocker dose due to AV-block, right ventricular pacing should be avoided. Currently, no data are available supporting biventricular pacing or HISpacing to enable a beta-blocker therapy in this population.
– In patients not tolerating beta-blockers who have left bundle branch block (>130 ms) and severe heart failure, biventricular pacing should be considered.

В настоящее время проходит рандомизированное исследование PACE-MI trial (см. статьи в приложении), оценивающее, имеет ли терапия бета-блокаторами при имплантации кардиостимулятора преимущества над отсутствием бета-блокаторов и кардиостимулятора у пациентов после инфаркта миокарда с противопоказанием к бета-блокаторам или симптоматической брадикардией на фоне приема бета-блокаторов.

[chUmNick]

Однозначно - нефизиологичная желудочковая стимуляция с постоянным ВА-проведением. И синдром кардиостимулятора.