جهت مشاوره و پاسخگويي به شما علاقمندان رشته الكتروفيزيولوژي و همچنين بيماران داراي بيماري هاي قلب و عروق و يا افرادي كه به آنان مطالعه الكتروفيزيولوزي قلب ويا ابليشن توصيه شده است وياپيس ميكر يا دفيبريلاتور داخلي دارند از تعدادي از پزشكان متخصص قلب و عروق و فوق تخصص الكتروفيزيولوژي قلب ياري جسته ايم.اميدواريم كه بتوانيم سهمي هرچند كوچك در ارتقا سطح علمي همكاران عزيز داشته باشيم و كمكي هر چند كوچك در بهبود و آسايش خاطر بيماران گرامي داشته باشيم.

پزشكان محترمي كه قبول زحمت نموده اند

آقاي دكتر هادي فدوي متخصص قلب و عروق و فوق تخصص الكتروفيزيولوزي قلب

آقاي دكتر عبدالحسين سوداگر  متخصص قلب و عروق و فوق تخصص الكتروفيزيولوزي قلب

آقاي دكتر اسفنديار فولادي متخصص قلب و عروق و  فوق تخصص الكتروفيزيولوزي قلب

 همچنين براي بيماران عزيز اين امكان فراهم شده است تا از طريق سايت ذیل مشاوره اینترنتی مستقیم با پزشک داشته باشند.برروی سایت اریتمی کلیک کنید

                        سایت آریتمیwww.epiran.com

 http://emedicine.medscape.com/article/151456-overview

Atrial tachycardia is a rhythm disturbance that arises in the atria. Atrial tachycardia can be observed in persons with normal hearts and in those with structurally abnormal hearts, including those with congenital heart disease and particularly after surgery for repair or correction of congenital or valvular heart disease.

Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for initiation and maintenance of the tachycardia. In common with most of the SVTs, the ECG typically shows a narrow QRS complex tachycardia (unless bundle branch block aberration occurs). Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular. The conducted ventricular rhythm is also usually regular but may become irregular, often at higher atrial rates because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckebach AV block.

The P wave morphology as observed on the ECG may give clues to the site of origin and mechanism of the atrial tachycardia. In the case of a focal tachycardia, the P wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the case of macroreentrant circuits, the P wave morphology and axis depend on activation patterns (see Workup).

Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than 100 bpm. Atrial activity is well organized, with at least 3 morphologically distinct P waves, irregular P-P intervals, and an isoelectric baseline between the P waves. Shine et al first proposed this definition in 1968.^[1] Multifocal atrial tachycardia has previously been described by names such as chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT. Go to Multifocal Atrial Tachycardia for more complete information on this topic.

A number of methods are used to classify atrial tachycardia, including origin as based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.

Based on endocardial activation, atrial tachycardia may be divided into 2 groups. The first is focal atrial tachycardia, which arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. The second group is the reentrant atrial tachycardias. These reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease, complex heart disease, and particularly after surgery involving incisions or scarring in the atria (see Clinical Presentation).

Atrial tachycardia may be classified according to the following pathophysiologic mechanisms: enhanced automaticity, triggered activity, or reentry (see Pathophysiology). Anatomical classification of atrial tachycardia is based on the location of the arrhythmogenic focus (see Anatomy).

A 12-lead electrocardiogram (ECG) is an important tool to help identify, locate, and differentiate atrial tachycardia. Laboratory studies may be indicated to exclude systemic disorders that may be causing the tachycardia. Electrophysiologic study may be required (see Workup).

The primary treatment during a bout of atrial tachycardia is considered to be rate control using AV nodal blocking agents, such as beta-blockers or calcium channel blockers (see Medication). Cardioversion should be considered for any patient in whom the rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective or contraindicated. Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and effective treatment option for symptomatic, medically refractory patients or those who do not desire long-term antiarrhythmic therapy. (see Treatment and Management.)

Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using Ensite mapping system. This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note the negative P waves in leads III and aVF (upright arrows) are different from the sinus beats (downward arrows). The RP interval exceeds the PR interval during the tachycardia. Note also that the tachycardia persists despite the atrioventricular block. Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atrioventricular nodal reentry tachycardia and atrioventricular tachycardia via an accessory pathway. Note also that the change in the P wave axis at the onset of tachycardia makes sinus tachycardia unlikely. Anterior-posterior projection is shown. An example of activation mapping using contact technique and EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium thought the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. TV – Tricuspid valveCS – Shadow of the catheter inserted in the coronary sinus Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. The local electrograms in the successful site preceded the surface P wave by 51 ms, consistent with successful site. Note that postablation electrograms on the ablation catheter is inscribed well past the onset of sinus rhythm P wave. The first 3 tracings show surface electrocardiograms as labeled.CS – Respective pair of electrodes of the coronary sinus catheterCS 7,8 – Located at the os of the coronary sinusCS 1,2 – Distal pair of electrodes Abl – Ablation catheter (D-distal pair of electrodes) An example of rapid atrial tachycardia mimicking atrial flutter. Single radiofrequency application terminates the tachycardia. The first 3 tracings show surface electrocardiograms, as labeled. HRA – High right atrial catheterRVA – Catheter located in right ventricular apexHBED and HBEP – Respectively, distal and proximal pair of electrodes in the catheter located at His bundleAblD and AblP – Respectively, distal and proximal pair of electrodes of the mapping catheterMAP – Unipolar electrograms from the tip of the mapping catheter

Atrial flutter (AFL) is an abnormal heart rhythm that occurs in the atria of the heart.^[1] When it first occurs, it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute),^[2] and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (e.g. hypertension, coronary artery disease, and cardiomyopathy), it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation (AF). However, it does rarely persist for months to years

In appropriate sinus tachycardia

حالتی است که در ان میزان ضربان قلب با کوچکترین فعالیتی 140 تا

 150 bpm است در هنگام استراحت حدود 100bpm  ودر هنگام خواب

بین 80-90 bpm  است.فرد با کمترین فعالیتی دچار طپش قلب،

سرگیجه و یا تنگی نفسريا افت فشار خون هنگام ایستادن و تعریق  و

طبیعتا اضطراب و ناراحتی  میشود.در نوار قلب این افرا هیچ انورمالی

هدایتی مشاهده نمیشودبرای تشخیص کامل این حالت ابتدا بایستی

بیماری هایی که تاکیکاردی سینوسی می دهند را رد کرد مانند بیماری

هایپر تیروییدی-سو مصرف برخی مواد-دیابت و

فیوکروموسیتوما...همچنین می باید بین این حالت و SVT  تمایز

نمود.این حالت بیشتر در خانم ها ی بین 20-30 سال شایع می

باشد.علت ان به درستی معلوم نیست برخی ان را ناشی از بیماری

گره سینوسی و برخی ناشی از اختلال در سیستم عصبی اتوماتیک

میدانند.

روش های درمان

1-در مان دارویی:بتا بلاکرها معمولا اثر خوبی دارند-  کلسیم بلاکر ها

نیز می توانند  فعالیت گره سینوسی راکم کنند

2-ابلیشن: با تعدیل modify  یا ابلیشن گره سینوسی انجام میشود در

کاتتر ابلیشن سیگنالی را اندتخاب میکنند A  activation  از همه  early 

 تر باشد.این عمل در 80 % موارد موفقیت امیز بوده ولی قابل ذکر است

که ریسک عود ان نیز بالا می باشد

3-افزایش میزان نمک خوراکی برای حفظ حجم خون در گردش که باید با

مشورت پزشک معالج باشد

4-برخی از پزشکان معتقدند که این بیماران نیاز به مداخله خاصی

ندارند چون با افزایش سن نشانه های بهبودی افزایش میابد

What is Inappropriate Sinus Tachycardia?

Inappropriate sinus tachycardia (IST) is a condition in which an individual's resting heart rate is abnormally high (greater than 100 beats per minute), their heart rate increases rapidly with minimal exertion, and their rapid heart rate is accompanied by symptoms of palpitations, fatigue, and exercise intolerance. IST is not associated with an abnormal electrical pattern on the ECG. The heart rhythm in IST appears to arise from within the sinus node, the cardiac structure that generates the normal heart rhythm. (Click here for a quick and easy review of the normal heart rhythm.)

What are the characteristics of IST?

While IST can be seen in anybody, it is most often a disorder of young women. The average IST sufferer is a woman in her late 20s or early 30s who has been having symptoms for months to years. In addition to the most prominent symptoms of palpitations, fatigue and exercise intolerance, IST can also be associated with a host of other symptoms including a drop in blood pressure upon standing, blurred vision, dizziness, tingling, shortness of breath, and sweating.

These patients most often have a resting heart rate of greater than 100 beats per minute, but it characteristically drops to 80 – 90 beats per minute while they are asleep. With even minimal exertion, the heart rate rapidly accelerates to 140 – 150 beats per minute. Palpitations (an unusual awareness of the heart beat) are a prominent symptom even though (as is often the case) there are no “abnormal” heart beats occurring. The symptoms experienced by sufferers of IST can be quite disabling and anxiety-producing.

IST was recognized as a syndrome only as recently as 1979, and has been generally accepted as a true medical entity only for the past 10 years or so. And even today, while IST is fully recognized as a genuine medical condition by every university medical center, many practicing physicians either haven’t heard of it or write it off as a psychological problem.

What causes IST?

Nobody knows.

The main question seems to be whether IST represents a primary disorder of the sinus node, or whether it represents a more general derangement of the autonomic nervous system – a condition called dysautonomia. Click here for a general description of the dysautonomia disorders.

Patients with IST are hypersensitive to adrenaline, such that a little bit of adrenaline (like a little bit of exertion) causes a marked rise in heart rate. There is evidence that the sinus node itself has structureal changes. But much other evidence suggests that a more general dysautonomia is present in these patients. (This would explain why symptoms most often seem out of proportion to the increase in heart rate.)

It is the notion that the sinus node itself is intrinsically abnormal that has led electrophysiologists to resort to ablation of the sinus node as a treatment for IST (more on this below).

What else needs to be considered in diagnosing IST?

Several other specific and treatable medical disorders can be confused with IST, and in a patient presenting with an abnormal sinus tachycardia, these other causes need to be ruled out. These disorders include hyperthyroidism, pheochromocytoma, diabetes-induced autonomic dysfunction, and substance abuse. These conditions generally can be ruled out with blood and urine tests.

In addition, other abnormal heart rhythm disorders – various types of SVT – can sometimes be confused with sinus tachycardia. Such SVTs need to be ruled out, because they can often be treated quite definitively.

http://www.wikidoc.org/index.php/T_wave_alternans

برای دیدن مطلب کامل در مورد T wave alternans بر روی لینک فوق کلیک کنید

T-wave alternans is a beat-to-beat alternation in the repolarization cycle of the heartbeat. It can be observed in the electrocardiogram (ECG) as a difference in the amplitude and morphology of the ST-segment and/or the T wave among successive odd and even beats in an ABAB pattern (Figure).

سیگنال اوریج SAECG

در قسمت الکتروفیزیولوژی برای اندازه گیری ventricular late potential  به کار میرود.امواج  late potential  به اندازه 1-25   میکروولت و در صورت وجود در انتهای  کمپلکس  QRS  وجود دارند.و برای تشخیص بیمارانی که در معرض  خطر تاکیکاردی بطنی خود به خود متعاقب انفارکتوس میوکارد و یا بروز SVT بر اثر تحریک الکتریکی ،مفید است. دستگاه سیگنال اوریج در حقیقت این امواج را تقویت،ثبت  و مقایسه کرده سیگنال های ناشی از پارازیت را حذف کرده و معیار ها را بیان میکند مقادیر نرمال اندازه گیری در ذیل آمده است

HFLA: high frequency,low amplitude<39

QRS duration: male< 114       female<120

RMSO4: root mean square>20

 پروسیجر غیر تهاجمی است و مراحل ان مانند گرفتن نوار قلب است. مدت ان 20  دقیقه است و در طی این مدت بیمار بر روی تخت خوابیده است .محل قرار گیری الکترود ها در برخی از دستگاه ها با نوار قلب متفاوت است و در سینه، گردن و پشت قفسه سینه قرار میگیرد.آمادگی خاصی قبل از انجام لازم نیست. بهترکه سینه بیماران تمیز و شیو شده باشد .سیگنال اوریج در بیمارانی که ریتم انها  PVC  زیاد دارد و بیمارانی که پیس دارند قابل قبول نیست.سایر کاربرد های سیگنال اوریج در متن انگلیسی ذکر شده است که در صورت علاقه مطالعه شود.

Signal-Average Electrocardiogram

(Signal-Averaged ECG, Signal-Averaged EKG, SAECG)

Procedure Overview

What is a signal-averaged electrocardiogram?

An electrocardiogram (ECG or EKG) is one of the simplest and fastest procedures used to evaluate the heart. Electrodes (small, plastic patches) are placed at certain locations on the chest, arms, and legs. When the electrodes are connected to an ECG machine by lead wires, the electrical activity of the heart is measured, interpreted, and printed out for the physician's information and further interpretation.

A signal-averaged electrocardiogram is a more detailed type of ECG. During this procedure, multiple ECG tracings are obtained over a period of approximately 20 minutes in order to capture abnormal heartbeats which may occur only intermittently. A computer captures all the electrical signals from the heart and averages them to provide the physician more detail regarding how the heart’s electrical conduction system is working.

Signal-averaged ECG is one of several procedures used to assess the potential for dysrhythmias/arrhythmias (irregular heart rhythms) in certain medical situations.

Other related procedures that may be used to assess the heart include resting electrocardiogram (ECG), Holter monitor, exercise electrocardiogram (ECG), cardiac catheterization, chest x-ray, computed tomography (CT scan) of the chest, echocardiography, electrophysiological studies, magnetic resonance imaging (MRI) of the heart, myocardial perfusion scans, radionuclide angiography, and ultrafast CT scan. Please see these procedures for additional information.

The heart's electrical conduction system:

The heart is, in the simplest terms, a pump made up of muscle tissue. Like all pumps, the heart requires a source of energy in order to function. The heart's pumping action comes from an intrinsic electrical conduction system.

An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node), which is a small mass of specialized tissue located in the right atrium (right upper chamber) of the heart.

The sinus node generates an electrical stimulus regularly at 60 to 100 times per minute under normal conditions. This electrical stimulus travels down through the conduction pathways (similar to the way electricity flows through power lines from the power plant to your house) and causes the heart's lower chambers to contract and pump out blood. The right and left atria (the two upper chambers of the heart) are stimulated first and contract a short period of time before the right and left ventricles (the two lower chambers of the heart).

The electrical impulse travels from the sinus node to the atrioventricular (AV) node, where impulses are slowed down for a very short period, then continues down the conduction pathway via the “bundle of His” into the ventricles. The “bundle of His” divides into right and left pathways to provide electrical stimulation to both ventricles.

This electrical activity of the heart is measured by an electrocardiogram. By placing electrodes at specific locations on the body (chest, arms, and legs), a graphic representation, or tracing, of the electrical activity can be obtained. Changes in an EKG from the normal tracing can indicate one or more of several heart-related conditions.

Reasons for the Procedure

Reasons your physician may request a signal-averaged ECG may include, but are not limited to, the following:

• to determine the cause of chest pain
• to evaluate other signs and symptoms which may be heart-related, such as fatigue, shortness of breath, dizziness, or fainting
• to help identify irregular heartbeats
• for further evaluation of dysrhythmias/arrhythmias noted on resting ECG

There may be other reasons for your physician to recommend a signal-averaged ECG.

Risks of the Procedure

A signal-averaged ECG is a quick, noninvasive method of assessing the heart’s function. Risks associated with ECG are minimal and rare.

Prolonged application of the adhesive electrode patches may cause tissue breakdown or skin irritation at the application site.

There may be other risks depending upon your specific medical condition. Be sure to discuss any concerns with your physician prior to the procedure.

Certain factors or conditions may interfere with or affect the results of the test. These include, but are not limited to, the following:

• obesity, pregnancy, or ascites (accumulation of fluid in the abdomen)
• anatomical considerations such as the size of the chest and the location of the heart within the chest
• movement during the procedure
• exercise, intake of high-carbohydrate meal, and/or smoking prior to the procedure
• certain medications
• electrolyte abnormalities, such as too much or too little potassium, magnesium, and/or calcium in the blood

Before the Procedure

• Your physician or the technician will explain the procedure to you and offer you the opportunity to ask any questions that you might have about the procedure.
• Generally, fasting is not required before the test.
• Notify your physician of all medications (prescribed and over-the-counter) and herbal supplements that you are taking.
• Notify your physician if you have a pacemaker.
• The area(s) where the electrodes are to be placed may be shaved.
• Based upon your medical condition, your physician may request other specific preparation.

During the Procedure

A signal-averaged ECG may be performed on an outpatient basis or as part of your stay in a hospital. Procedures may vary depending on your condition and your physician’s practices.

Generally, a signal-averaged ECG follows this process:

1. You will be asked to remove any jewelry or other objects that may interfere with the procedure.
2. You will be asked to remove clothing from the waist up. The technician will ensure your privacy by covering you with a sheet or gown and exposing only the necessary skin.
3. You will lie flat on a table or bed for the procedure. It will be important for you to lie still and not talk during the procedure, so as not to interfere with the tracing.
4. If your chest is very hairy, the technician may shave small patches of hair, as needed, so that the electrodes will stick closely to the skin.
5. Electrodes will be attached to your chest, abdomen, and back.
6. The lead wires will be attached to the skin electrodes.
7. Once the leads are attached, the technician may key in identifying information about you into the machine's computer.
8. The EKG will be started. Generally, it will take about 20 minutes to obtain the necessary ECG information.
9. Once the tracing is completed, the technician will disconnect the leads and remove the skin electrodes.

After the Procedure

You should be able to resume your normal diet and activities, unless your physician instructs you differently.

Generally, there is no special care following a signal-averaged ECG.

Notify your physician if you develop any signs or symptoms you had prior to the test (e.g., chest pain, shortness of breath, dizziness, or fainting).

Your physician may give you additional or alternate instructions after the procedure, depending on your particular situation.

اختلال الکتروکاردیوگرافی سندرم Wolf Parkinson White (WPW زمانی به وجود می آید که تحریک دهلیزی تمام یا قسمتی از بطن ها یا تحریک بطنی، تمام یا قسمتی از دهلیز را زودتر از زمانی فعال کند که از انتقال تحریک از مسیر هدایتی تخصیص یافته طبیعی انتظار می رود. این فعال شدن زودرس به وسیله ارتباطات عضلانی ایجاد می شود که در حقیقت فیبرهای میوکاردی هستند که در خارج از بافت هدایتی تخصیص یافته قرار دارند و مسیرهای فرعی نامیده می شوند. به این اختلال زمانی سندرم تلقی می شود که به علت وجود مسیر فرعی، تاکی آریتمی ایجاد گرد

بروز سندرم ولف پارکینسون وایت تا 3 در هزار هم گزارش شده است. اغلب افراد مبتلا به سندرم WPW قلب سالم دارند و بروز تاکی آریتمی ها می تواند حیات آ نها را به خطر اندازد و حتی احتمال وقوع مرگ ناگهانی با فرکانس تخمینی 1/0% وجود دارد. تعدد تاکی کاردهای حمله ای با افزایش سن بیشتر می شود.

در زمینه انتخاب درمان، درمانهای دارویی آنتی آریتمیک از زمانهای قدیم برای سندرم WPW وجود داشته و هر چند با موفقیت هایی همراه بوده، اما کاملاً مطلوب نبوده است. با مصرف این داروها کاهش در بروز مرگ ناگهانی قابل پیش بینی نبوده و در مصرف کوتاه مدت و درازمدت، عوارض متعددی ایجاد می گردد. امروزه برای بررسی تشخیص و درمان آریتمی ها بررسی الکتروفیزیولوژیک قلب (EPS) Electro Physiologic Study و استفاده از انرژی رادیوفرکونسی، نقش عمده ای پیدا نموده است. در مطالعات انجام شده، (Radiofrequency Catheter Ablation) RFCA زمانی که توسط الکتروفیزیولوژیست های بالینی ماهر انجام گردیده، بسیار بی خطر و نتایج عالی به همراه داشته است اثربخشی، بی خطری و به صرفه بودن این روش درمانی، آن را به درمان انتخابی تبدیل کرده است

بیماران ممکن است علایمی چون طپش قلب،درد قفسه سینه، سنکوپ،SCD  را تجربه نمایند

در الکتروکاردیوگرام شاهد وجود  PR interval  کوتاه – موج دلتا – افزلیش اندازه  QRS  هستیم.

تاکی کاردی در WPW به دو صورت ارتودرومیک( طرح  LBBB  ) و یا انتی درومیک ( طرح  RBBB ) در  V1 است.

در تعیین محل WPW الکتروکاردیوگرام هم می تواند کمک کننده و هم گمراه کننده باشد . معمولا در انهایی که دلتای کوچک دارند مسیر فرعی در سمت چپ  ودر دلتاهای بزرگ مسیر فرعی در سمت راست است ( این یک اصل کلی نیست).هنگامی که دلتا هست  HV کوتاه تر میشود.

 راهنمای مکان های مسیر فرعی:

Right free wall: دلتای مثبت در لید  I and avL به همراه  LEFT axis

Right antroseptal : دلتای مثبت در لید II – III  -avF

Left Free Wall : دلتای منفی در لید avL – I – V5 –V6   

Typical Right Postroseptal : دلتای ایزوالکتریک در  avF – III – II  و  وجود  rS در  V1  - وجود  Rs در  V2

نسبت  این دو موج در V1 –V2  تغییر میکند.(

.( transient zone

Right Postro Septal: دلتای منفی در لید II – III – avF