Tóm tắt hướng dẫn của Acc/Aha/Hrs 2015 cho điều chỉnh nhịp nhanh trên thất ở người lớn – P3

8. Nhịp nhanh bộ nối (Junctional Tachycardia)

Xem hình 12 thuật toán điều chỉnh tiếp tục nhịp nhanh bộ nối và Tư liệu Hỗ trợ online 18 và 19 cho tư liệu bỏ xung phần 8.

TS Phạm Hữu Văn

Hình 12 điều chỉnh liên tục nhịp nhanh bộ nối. Các màu tương xứng với Class các Khuyến cáo ở bẳng 1; các thuốc được liệt kê theo alphabe. SHD chỉ bệnh tim cấu trúc (gồm bệnh tim thiếu máu cục bộ)

Nhịp nhanh bộ nối (được định nghĩa ở bảng 2) là nhịp nhanh phức bộ hẹp, đôi khi không đều (với tần số thường 120 bpm đến 220 bpm) phát sinh từ bộ nối AV (gồm cả bó His). Phân ly AV (thường đồng nhịp) có thể được nhìn thấy, khi biểu hiện, loại trừ chẩn đoán sai của AVRT và làm khó chẩn đoán AVNRT. Nếu không đều, nhịp nhanh bộ nối có thể chẩn đoán nhầm với AF hoặc MAT. Cơ chế nhịp nhanh bộ nối do tính tự động gia tăng (bất thường) từ ổ ngoại vị trong bộ nối AV (gồm cả bó His) ^[275]

Nhịp nhanh bộ nối ít gặp ở người lớn ^[275]; loạn nhịp này thường được thấy ở trẻ sau phẫu thuật, sau khi phẫu thuật tim cho bệnh tim bẩm sinh; điều này còn được biết như nhịp nhanh ngoại vị bộ nối. Như vậy, có bằng chứng hạn chế liên quan đến chẩn đoán và điều chỉnh nhịp nhanh bộ nối ở các bệnh nhân người lớn.

Nhịp nhanh bộ nối nhịp có liên quan, không thành cơn (thường được biết nhiều hơn như nhịp bộ nối AV gia tăng), nhịp nhanh kịch phát bộ nối phổ biến ở người lớn hơn. Cơ chế của nhịp nhanh bộ nối không thành cơn được kết hợp với tính tự động gia tăng hoặc hoạt động khởi kích (triggered). Nó xảy ra ở tốc độ chậm hơn (70 bpm đến 130 bpm) và thường do nhiễm độc digoxin ^[276] hoặc nhồi máu cơ tim.^[277,278]. Điều trị nhịp này tập trung chú ý vào trạng thái nền.

8.1. Điều trị cấp thời: Các khuyến cáo

Các khuyến cáo cho điều trị cấp thời nhịp nhanh bộ nối (KC 1)

8.2. Điều chỉnh tiếp tục: Các khuyến cáo

Khuyến cáo điều chỉnh tiếp tục nhịp nhanh bộ nối (KC 2)

9. Các quần thể đặc biệt

9.1. Nhi khoa

Như đã thảo luận trong mục 1.4, các tài liệu này nhằm vào dân số trưởng thành (≥18 tuổi) và không cung cấp các khuyến cáo cụ thể cho bệnh nhân nhi. Tuy nhiên, một cuộc thảo luận ngắn gọn về SVT ở bệnh nhi được bao gồm bên dưới, làm nổi bật những cân nhắc chính đối với SVT ở bệnh nhân trẻ hơn, trong đó có bệnh nhân vị thành niên.

SVT ở những bệnh nhân trẻ tuổi khác với SVT ở người lớn một cách đáng kể về giới hạn cơ chế, nguy cơ phát triển suy tim hoặc ngừng tim, nguy cơ liên quan với liệu pháp can thiệp, bệnh sử tự nhiên và tác động tâm lý xã hội. Khoảng một nửa số SVT nhi biểu hiện trong 4 tháng đầu tiên của đời sống, với đỉnh liên quan đến tuổi trong lần xuất hiện sau đó ở 5 đến 8 tuổi và sau 13 tuổi. Nhịp nhanh qua trung gian đường phụ chiếm khoảng > 70% các SVT ở trẻ sơ sinh, giảm xấp xỉ 55% ở thanh thiếu niên^{. [21,289-291]} AVNRT tăng theo độ tuổi, từ 9% đến 13% các SVT ở trẻ sơ sinh, 30% đến 50% của SVT ở thanh thiếu niên. Cuồng nhĩ được gặp trong một số trẻ sơ sinh và trẻ em lớn tuổi chủ yếu được quan sát thấy sau các bệnh tim bẩm sinh. AF không phổ biến ở trẻ em, chiếm < 3% các loạn nhịp trên thất và có thể là hậu quả của AVRT hoặc AVNRT ở thanh thiếu niên hoặc có thể liên quan với bệnh tim bẩm sinh được sửa chữa. Suy tim sung huyết biểu hiện đến 20% trẻ sơ sinh và trẻ em lớn tuổi với nhịp nhanh liên hồi và trong những trường hợp hiếm hoi có thể cần hỗ trợ tim cơ học trong quá trình điều trị khởi đầu. ^[292]

Nguy cơ rung thất hoặc SCD liên quan đến WPW ở trẻ em là 1,3% đến 1,6% và là mức cao nhất trong 2 thập kỷ đầu tiên của đời sống.^[23,165-168] Nguy cơ ngừng tim là cao hơn ở những bệnh nhân với AVRT thúc đẩy AF, giai đoạn trơ đường nối phụ ngắn và các đường phụ sau vách.^[23,165-168] Điều trị thuốc SVT ở trẻ em được dựa trên các mẫu thực hành rộng lớn điều trị các thuốc chống loạn nhịp trong các RTC còn đang thiếu. Các thuốc block nút AV đã được sử dụng rộng rãi cho đại đa số loạn nhịp, AVRT và AVNRT. Các liều khởi đầu adenosine cao hơn được cần thiết ở trẻ em hơn ở người lớn, trẻ em nhận được từ 150 mcg / kg đến 250 mcg / kg.^[293-295] Digoxin tránh sử dụng khi có kích thích sớm do việc sử dụng trong giai đoạn trẻ nhỏ được kết hợp với SCD hoặc VF. ^[296,297] Amiodarone, sotalol, Propafenone, hoặc flecainide có thể được sử dụng cho SVT trơ ở trẻ sơ sinh. Ở trẻ lớn hơn có biểu hiện SVT, điều trị beta-blocker được sử dụng thông thường nhất cho điều trị khởi đầu. Do sự xuất hiện hiếm hoi các biến cố bất lợi của flecainide, kể cả ở những bệnh nhân không có bệnh tim cấu trúc, flecainide không được sử dụng như một thuốc hàng đầu ở trẻ em.^[298]

Triệt phá qua catheter có thể được thực hiện thành công ở trẻ em ở mọi lứa tuổi, với tỷ lệ thành công cấp thời so sánh với những báo cáo ở người lớn. ^{[192.193.299.300]} Các biến chứng đã được báo cáo ở 4% đến 8% của loạt lớn khởi đầu, với các biến chứng lớn ở 0,9% đến 3,2% và tỷ lệ biến chứng cao hơn ở bệnh nhân cân nặng <15 kg.^{[192,299-301]} Các tác động của biến chứng, gồm cả block AV đòi hỏi tạo nhịp, thủng tim và động mạch vành hoặc tổn thương van hai lá nặng ở những bệnh nhân trẻ. ^[302-304] Ở loạt đầu, tử vong đã được báo cáo ở 0,12% trẻ em tim bình thường và kết hợp với trọng lượng thấp hơn và tăng số lượng các tổn thương triệt phá. ^[305] Mặc dù hầu hết các trung tâm thực hiện triệt phá chọn lọc cho các trẻ em cân nặng > 12 kg đến 15 kg, triệt phá ở người trẻ hơn hoặc trẻ nhỏ hơn thường được dành cho những bệnh nhân có SVT trơ với thuốc hoặc bệnh cơ tim do nhịp nhanh gây ra hoặc trước khi phẫu thuật có thể hạn chế tác động cho các thủ thuật trên cơ sở catheter tiếp theo.

Nhịp nhanh ngoại vị bộ nối (Junctional ectopic tachycardia) xảy ra chủ yếu ở những bệnh nhân rất trẻ, hoặc như là một hình thức bẩm sinh, hoặc thường hơn, sau khi sửa chữa bệnh tim bẩm sinh. Nhịp tim nhanh bộ nối không phải sau phẫu thuật (Nonpostoperative junctional tachycardia) đã được báo cáo đáp ứng với amiodarone hoặc trị liệu hỗn hợp gồm các thuốc beta blockers, flecainide, procainamide, hay propafenone. ^[306] Triệt phá cho những bệnh nhân có nhịp tim nhanh trơ hoặc rối loạn chức năng thất đã cho thấy hiệu quả 82% đến 85%, nhưng block AV ngẫu nhiên xảy ra ở 18% và tái phát đã được thấy ở 14% số bệnh nhân.^[306] Nhịp nhanh bộ nối sau phẫu thuật xảy ra ở 2% đến 10% số bệnh nhân trẻ tuổi được phẫu thuật bên trong tim.^[307.308] Điều trị gồm thuốc giảm đau với giãn cơ, hạn chế các loại thuốc inotrop, giảm nhiệt độ cơ thể để 34 đến 35°C, tạo nhịp nhĩ vượt tần số, procainamide hoặc truyền amiodarone. ^[309-313] Nói chung, giải quyết nhịp nhanh bộ nối sau phẫu thuật và không cần điều trị tiếp tục.

Mặc dù hướng dẫn này tập trung ở người lớn, cần lưu ý SVT có thể xảy ra cho thai nhi, nếu dai dẳng, có thể đưa thai nhi đến nguy cơ trụy tim mạch biểu hiện bằng ứ dịch toàn thân (hydrops). Các bà mẹ cần phải do các chuyên gia tim mạch người lớn theo dõi sự an toàn trong khi điều trị. Các cơ chế phổ biến nhất cho SVT thai nhi là AVRT và cuồng nhĩ. ^[314] SVT dai dẳng với ứ dịch toàn thân có tỷ lệ tử vong cao, do đó, đảm bảo điều trị kịp thời và tích cực. Sử dụng các thuốc chống loạn nhịp cho mẹ đã nhận thấy có ảnh hưởng qua nhau thai.

9.2. Các bệnh nhân có bệnh tim bẩm sinh người lớn

Xem Hình 13 cho các thuật toán để điều trị cấp thời SVT không có kích thích sớm ở các bệnh nhân tim bẩm sinh người lớn (adult congenital heart disease: ACHD); Hình 14 cho các thuật toán điều chỉnh tiếp tục SVT không có kích thích sớm các bệnh nhân ACHD; tư liệu trực tuyến bổ sung 20 và 21 cho tư liệu hỗ trợ Phần 9.

Hình 13. Điều trị SVT cấp thời ở bệnh nhân nhi. Các màu sắc tương ứng với các khuyến cáo ở bảng 1; các thuốc được liệt kê theo alphabe. BN: chỉ bệnh nhân. * Đối với những nhịp tự cắt hoặc tái lại tự phát, chuyển nhịp đồng bộ không thích hợp. ACHD: bệnh tim bẩm sinh người lớn; IV: tiêm tĩnh mạch; SVT: nhịp nhanh trên thất.

Hình 14 điều chỉnh tiếp tục SVT ở các bệnh nhân nhi. Các màu tương ứng mức độ các khuyến cáo ở bảng 1; các thuốc được liệt kê theo alphabe. ACHD chỉ bệnh tim bẩm sinh ở người lớn; SVT chỉ nhịp nhanh trên thất.

9.2.1. Các đặc tính lâm sàng

SVT thấy ở 10% đến 20% bệnh nhân ACHD và được liên kết với một nguy cơ gia tăng đáng kể suy tim, đột quỵ, và SCD. ^[315-319] Cơ chế phổ biến nhất của SVT ở bệnh nhân ACHD là nhịp nhanh nhĩ vào lại vòng lớn (macroreentrant AT) (còn gọi là cuồng (flutter)), chiếm ít nhất 75% SVT và thường xuyên liên quan đến việc CTI (cavotricuspid isthmus). AT ổ, AVNRT và nhịp nhanh qua trung gian đường phụ mỗi loại chiếm dưới 8% SVT, trong khi tỷ lệ AF khoảng 10% và tăng theo tuổi. ^[320-325]

Việc điều chỉnh SVT ở bệnh nhân ACHD chịu ảnh hưởng của giải phẫu cơ tim và phẫu thuật sửa chữa, di chứng huyết động hiện tại của sửa chữa giải phẫu và cơ chế của SVT. Điều chỉnh bệnh nhân ACHD cần được thực hiện chỉ trong sự hợp tác với một bác sĩ tim mạch có đào tạo chuyên sâu hoặc kinh nghiệm trong việc điều chỉnh các bệnh nhân này.

Tỷ lệ thành công cấp thời toàn bộ của thủ thuật triệt phá SVT ở bệnh nhân ACHD dao động từ 70% đến 85%, với tái phát ở 20% đến 60% bệnh nhân trong vòng 2 năm. ^[326-331] Triệt phá qua catheter được thách thức do những hạn chế tiếp cận tĩnh mạch vào tim, tổ chức nhĩ đã phì đại, vòng vào lại ở nhĩ phức tạp và các vách ngăn tâm nhĩ phân vùng xoang vành và CTI đến nhĩ tĩnh mạch phổi. Sự phát triển rối loạn nhịp nhĩ ở bệnh nhân ACHD thường là dấu hiệu của sự thay đổi huyết động tiến triển, đòi hỏi đánh giá chức năng và huyết động chuyên sâu. Can thiệp vào các khiếm khuyết huyết động / chức năng tồn dư có thể cần được lên kế hoạch như là một phần của điều chỉnh loạn nhịp lâu dài.

9.2.2. Điều trị cấp thời: Các khuyến cáo

Các khuyến cáo điều trị cấp thời SVT ở bệnh nhân ACHD (KC 3)

9.2.3. Điều chỉnh tiếp tục: Các khuyến cáo

Các khuyến cáo điều chỉnh tiếp tục SVT ở các bệnh nhân ACHD (KC 4)

9.3. Thai nghén

Mang thai có thể có nhạy cảm tăng lên đối với một loạt các rối loạn nhịp, ngay cả trong trường hợp không có bệnh tim. ^[378] Mang thai cũng có liên quan với tăng nguy cơ loạn nhịp tim trầm trọng, chẳng hạn các cơn nhịp tim nhanh thường xuyên hơn và trơ hơn, ở những bệnh nhân có nền kích thích sớm loạn nhịp. ^[379] Mặc dù có độc tính tiềm tàng cho thai nhi với một số liệu pháp dùng thuốc và không dùng thuốc, lựa chọn an toàn tồn tại để cho phép điều trị đại đa số các trường hợp hiệu quả SVT của mẹ.

Các tài liệu về các lựa chọn điều trị cho việc điều chỉnh rối loạn nhịp trong thai kỳ thường được giới hạn trong các báo cáo trường hợp đơn lẻ hoặc loạt nhỏ và ủng hộ sử dụng thuốc chống loạn nhịp cũ hơn do các báo cáo phong phú hơn về việc sử dụng an toàn của các loại thuốc này. Mặc dù tất cả các loại thuốc có tác dụng phụ tiềm tàng cho cả hai mẹ và thai nhi ở bất kỳ giai đoạn nào của thai kỳ, nếu có thể, các loại thuốc nên tránh dùng trong ba tháng đầu tiên, khi nguy cơ dị tật bẩm sinh lớn nhất. Liều thấp nhất được khuyến cáo nên được sử dụng khởi đầu, kèm theo theo dõi thường xuyên đáp ứng lâm sàng.

9.3.1. Điều trị cấp thời: Các khuyến cáo

Các khuyến cáo điều trị cấp thời SVT ở các bệnh nhân mang thai (KC 5)

9.3.2. Điều chỉnh tiếp tục: Các khuyến cáo

Khuyến cáo điều chỉnh tiếp tục SVT các bệnh nhân mang thai (KC 6)

9.4. SVT ở người lớn tuổi

9.4.1. Điều trị cấp thời và điều chỉnh tiếp tục: Các khuyến cáo

Bệnh sử tự nhiên của SVT được thay đổi đều đặn vì hầu hết các bệnh nhân SVT đã trải qua triệt phá ở độ tuổi trẻ hơn, nhưng nhìn chung, tỷ lệ tương đối của AT cao hơn trong các quần thể lớn tuổi và AVNRT phổ biến hơn AVRT trong số bệnh nhân trải qua triệt phá. ^[16] Cuồng nhĩ không điển hình và AT vào lại vòng lớn đang gia tăng như hậu quả của việc tăng triệt phá AF trong số bệnh nhân này, tuy nhiên có số liệu kết quả hạn chế từ RCT cho phân khúc này của quần thể. Các quyết định điều trị cần được cân bằng giữa nguy cơ và lợi ích toàn bộ các đặc tính xâm lấn của triệt phá đối lại với sự nhậy cảm của khả năng đáp ứng và hiệu quả lâu dài đối với trị liệu thuốc.

Các khuyến cáo điều trị cấp thời và điều chỉnh liên tục SVT ở quần thể lớn tuổi. (KC 7)

Bệnh nhân SVT có thể gặp các triệu chứng tái phát ảnh hưởng xấu đến chất lượng sống của họ. Các cơn nhịp tim nhanh có thể gây choáng váng và ngất, có thể trở thành một trở ngại cho việc thực hiện các hoạt động thông thường của cuộc sống hàng ngày (ví dụ, lái xe) .^[29] Tuy nhiên, có những dữ liệu tối thiểu về ảnh hưởng của điều trị đến chất lượng sống đối với bệnh nhân SVT .

Xem dữ liệu trực tuyến bổ sung 22 cho dữ liệu hỗ trợ Phần 10.

Phần nhỏ y văn đánh giá các chiến lược hiệu quả – chí phí trong PSVT đã được tập trung cơ bản vào đánh giá trị liệu thuốc đối lại với triệt phá qua catheter. Mô hình Markov hiệu quả – chi phí chính xác được thực hiện vào năm 2000 để so sánh triệt phá bằng tần số radio và điều chỉnh thuốc với chủng loại metoprolol từ quan điểm xã hội. ^[57] Quần thể được ước tính gồm bệnh nhân AVNRT (khoảng 65%) và AVRT. Trên cơ sở mô phỏng này, các tác giả kết luận, đối với các bệnh nhân có triệu chứng với cơn PSVT hàng tháng, triệt phá tần số radio là chiến lược hiệu quả hơn và ít tốn kém hơn khi so sánh với điều trị nội khoa. Một nghiên cứu thuần tập quan sát bệnh nhân cuồng nhĩ được hỗ trợ triệt phá sớm để làm giảm đáng kể việc sử dụng thuốc trong bệnh viện và các nguy cơ của AF. ^[397]

Những nghiên cứu này, cùng với các y văn trước đây khác, ưu tiên triệt phá qua catheter hiệu quả hơn trị liệu thuốc để điều trị PSVT và cuồng nhĩ. Tuy nhiên, kết quả của những nghiên cứu này dựa trên số liệu chi phí và mô hình thực hành mà không áp dụng cho môi trường hiện tại và thực hành. Do đó, không có khuyến cáo được cung cấp.

Xem dữ liệu trực tuyến bổ sung 23 cho dữ liệu hỗ trợ Mục 11.

12. Chia sẻ Quyết Định

Điều quan trọng bệnh nhân được đưa vào quá trình ra quyết định lâm sàng, với việc xem xét / sở thích và mục tiêu điều trị, cũng như / tình trạng thể chất, tâm lý và tình huống xã hội của bệnh nhân. Trong các trường hợp lựa chọn, được cá thể hóa, các can thiệp tự định hướng có thể được phát triển trong quan hệ đối với bệnh nhân, chẳng hạn như thủ pháp phế vị và thuốc điều trị “thuốc trong túi” (pill – in – the – pocket).

Quá trình ra quyết định đặc biệt quan trọng đối với bệnh nhân SVT. Như đã thấy trong hướng dẫn này, điều trị SVT có thể có khác biệt tinh tế và đòi hỏi phải có kiến thức chuyên môn về quá trình EP và lựa chọn điều trị. Lựa chon điều trị rất cụ thể cho loại rối loạn nhịp chính xác và có thể phụ thuộc vào đặc tính chắc chắn của rối loạn nhịp cụ thể. Các lựa chọn khác nhau để điều trị, bao gồm cả các loại thuốc, sốc, điều trị xâm lấn, hoặc kết hợp chúng, có thể gây nhầm lẫn cho người bệnh, do đó, một lời giải thích chi tiết về những lợi ích và rủi ro phải được bao gồm trong cuộc tư vấn.

Bệnh nhân được khuyến khích đặt câu hỏi với thời gian quy định cho những người chăm sóc để đáp ứng. Cung cấp bầu không khí thoải mái, dự đoán mối quan tâm bệnh nhân và khuyến khích bệnh nhân để giữ một quyển ghi chép với những câu hỏi có thể tạo điều kiện cho các cuộc trò chuyện dễ dàng.

Điều quan trong cho các bác sỹ lâm sàng sử dụng thuật ngữ đơn giản để giải thích các lựa chọn điều trị cho bệnh nhân. Đây là trách nhiệm của đội ngũ bác sĩ và y tế để cung cấp cho bệnh nhân với sự hiểu biết tốt nhất tất cả các lựa chọn điều trị với rủi ro, lợi ích và tác động tiềm tàng về chất lượng sống.

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