Tóm tắt hướng dẫn của Acc/Aha/Hrs 2015 cho điều chỉnh nhịp nhanh trên thất ở người lớn – P2

4. Nhịp nhanh nhĩ ổ không phải xoang và MAT

Xem hình 4 về thuật toán điều trị cấp thời nhịp nhanh nhĩ nghi ngờ ổ (AT). Hình 5 về thuật toán điều trị tiếp tục AT ổ và Tư liệu hỗ trợ trực tuyến 6, 7 và 8 cho các tư liệu hỗ trợ phần 4.

TS Phạm Hữu Văn

Hình 4 biểu thị thuật toán điều trị cấp thời nhịp nhanh nhĩ nghi ngờ ổ. Màu sắc tương ức với class khuyến cáo ở bảng 1; các thuốc được liệt kể theo abc.* Đối với nhịp tự mất đi hoặc tự tái phát, chuyển nhịp đồng bộ là không phù hợp. IV chỉ đường tĩnh mạch.

Hình 5 thể hiện thuật toán điều chỉnh tiếp tục nhanh nhĩ ổ. Các màu sắc tương ứng với Class khyến cáo ở bảng 1; các thuốc liệt kê theo abc. SHD: bệnh tim thực thế.

4.1. Nhịp nhanh nhĩ ổ

AT ổ được định nghĩa ở bảng 2. AT ổ có thể dai dẳng hoặc tạm thời. Tần số nhĩ trong quá trình AT ổ thường giữa 100 bpm và 250 bpm. [102] Sự có mặt và mức độ nặng của các triệu chứng trong quá trình AT ổ có thể thay đổi ở các bệnh nhân. AT ổ ở các quần thể người lớn thường kết hợp với tiến triển lành tính, mặc dù bệnh cơ tim qua trung gian AT đã được thông báo ở > 10% các bệnh nhân được đưa đến triệt phá do SVT liên hồi.[103,104] AT ổ tạm thời nói chung và thường không đòi hỏi điều trị.

Chẩn đoán AT ổ được nghi ngờ khi tiêu chuẩn có trên ECG (phần 2). Thuật toán đã được phát triển để xác định nguồn gốc AT ổ tử hình dạng sóng P được ghi trên 12 chuyển đạo ECG chuẩn. [^105,106] Định khu chính xác AT ổ được khẳng định cuối cùng bằng lập bản đồ trong quá trình EPs khi triệt phá thành công đã đạt được.[107–116] AT ổ có nguồn gốc thường hơn ở nhĩ phải so với nhĩ trái. [117,118]

Nhịp nhanh vào lại tại nút xoang là một type AT ổ ít gặp liên quan đến vòng vào lại vi thể ở khu vực nút xoang nhĩ, tạo ra hình thái sóng P giống hệt như nhịp xoang nhanh (mặc dù đây không phải nhịp xoang nhanh). Đặc điểm phân biệt vào lại nút xoang với nhịp xoang nhanh gồm khởi phát và cắt cơn đột ngột và thường khoảng RP dài hơn so với quan sát trong quá trình nhịp xoang bình thường.

4.1.1. Điều trị cấp thời: Các khuyến cáo

RCTs về điều trị thuốc để so sánh hiệu quả ở các bệnh nhân có AT ổ trong các tình huống cấp là không có khả năng. Nhiều kết quả lâm sàng đã được thông báo tử các nghiên cứu quan sát nhỏ bao gồm các bệnh nhân vị thành niên và nhi khoa.[119,120] Trong tình huống lâm sàng, nếu chẩn đoán không chắc chắn, thủ thuật cường phế vị có thể thử áp dụng để nhận biết tốt hơn cơ chế SVT. (KC 1)

Các khuyến cáo điều trị cấp thời nghi ngờ nhịp nhanh nhĩ ổ (KC 1)

4.1.2. Điều chỉnh tiếp tục: Các khuyến cáo (KC 2)

Các khuyến cáo cho điều chỉnh tiếp tục nghi ngờ nhịp nhanh nhĩ ổ (KC 2)

4.2. Nhịp nhanh nhĩ đa ổ (Multifocal Atrial Tachycardia: MAT)

MAT được định nghĩa ở Bảng 2. Cơ chế của MAT còn chưa được xác định rõ. MAT thường được kết hợp với các điều kiện nền, bao gồm bệnh phổi, tăng áp phổi, bệnh mạch vành, bệnh van tim, [137] cũng như giảm magiê máu và điều trị theophylline. [138] Việc điều trị đầu tiên là điều chỉnh trạng thái nền. Magiê tĩnh mạch cũng có thể hữu ích ở những bệnh nhân có nồng độ magiê bình thường. [139] Thuốc chống loạn nhịp nói chung không phải là hữu ích trong loại bỏ MAT. [140] Chuyển nhịp là không hữu ích trong MAT. [137]

4.2.1. Điều trị cấp thời: Khuyến cáo (KC 3)

Các khuyến cáo điều trị cấp thời nhịp nhanh nhĩ đa ổ (KC 3)

4.2.2. Điều chỉnh tiếp tục: Các khuyến cáo (KC 4)

Các khuyến cáo cho điều chỉnh tiếp tục nhịp nhanh nhĩ đa ổ (KC 4)

5. Nhịp nhanh vào lại nút nhĩ thất

Xem hình 6 cho thuật toán điều trị cấp thời AVNRT, hình 7 cho thuật toán điều chỉnh tiếp tục AVNRT, tư liệu Online bổ xung 9 và 10 cho tư liệu ủng hộ thêm phần 5.

Hình 6. Điều trị cấp thời AVNRT. Màu sắc tương ứng với class của Khuyến cáo trong Bảng 1; thuốc được liệt kê theo thứ tự abc. * Đối với những nhịp chấm dứt hoặc tái phát tự phát, chuyển nhịp đồng bộ là không thích hợp. AVNRT chỉ nhịp nhanh vào lại nhĩ thất; và IV: tiêm tĩnh mạch.

Hình 7. Điều trị tiếp tục AVNRT. Các màu tương ứng với Class của khuyến cáo trong bảng 1; các thuốc được liệt kê theo alphabe. AVNRT chỉ nhịp nhanh vào lại nút nhĩ thất; SHD chi bệnh tim cấu trúc (gồm bệnh tim thiếu máu cục bộ)

AVNRT là SVT phổ biến nhất và được định nghĩa ở bảng 2. Người ta thường gặp ở người trẻ không có bệnh tim thực thể hoặc bệnh tim thiếu máu cục bộ, > 60% các trường hợp gặp ở phụ nữ. [16] Tần số thất thường 180 bpm đến 200 bpm nhưng phạm vi từ 110 bpm đến >250 bpm (ở các trường hợp hiếm tần số có thể <100 bpm). [19] Nền giải phẫu của AVNRT là sinh lý nút AV hai đường (bảng 2).

5.1. . Điều trị cấp thời: Các khuyến cáo (KC 5)

Các  khuyến  cáo  cho điều  trị  cấp  thơì  AVNRT (KC 5)

5.2. Điều chỉnh tiếp tục: Các khuyến cáo (KC 6)

Các khuyến cáo cho điều chỉnh tiếp tục AVNRT (KC 6)

Các đường phụ (được xác định ở bảng 2) có thể tiến hành theo hướng xuôi (anterograde), hướng ngược (retrograde), hoặc cả hai; có thể được liên kết với một số loạn nhịp trên thất khác nhau. Một số đường xuôi có thể đặt bệnh nhân vào nguy cơ SCD.

Nhịp tim nhanh phổ biến nhất liên quan đến đường phụ là orthodromic AVRT, với vòng chu kỳ sử dụng các nút AV và hệ thống His – Purkinje theo hướng xuôi, tiếp theo dẫn truyền đến tâm thất, dẫn ngược theo đường phụ, hoàn thành vòng bằng dẫn truyền qua tâm nhĩ trở lại nút nhĩ thất. Orthodromic AVRT chiếm khoảng 90% đến 95% các cơn AVRT ở bệnh nhân có một đường phụ biểu hiện. AVRT được kích thích sớm, bao gồm antidromic AVRT, chiếm 5% trong các cơn AVRT ở bệnh nhân có một đường biểu hiện và liên quan đến việc dẫn truyền từ tâm nhĩ đến tâm thất thông qua con đường phụ, gây ra phức hợp QRS được kích thích sớm. Điều này được gọi là nhịp nhanh antidromic AVRT khi dẫn truyền vào lại trở lại biểu hiện ngược qua nút AV. Trong trường hợp hiếm của AVRT kích thích sớm, sự dẫn trở lại xảy ra thông qua một con đường AV phụ thứ hai. AF có thể xảy ra ở những bệnh nhân với các đường phụ, có thể dẫn đến dẫn truyền vô cùng nhanh đến tâm thất trên một đường biểu hiện, làm tăng nguy cơ gây rung thất và SCD.

Dẫn truyền xuôi nhanh qua đường phụtrong AF có thể dẫn đến SCD ở bệnh nhân có một đường phụ biểu hiện, với phạm vi nguy cơ 10 năm dao động từ 0,15% đến 0,24%. ^[164.165] Thật không may, SCD có thể được biểu hiện đầu tiên của bệnh nhân với chẩn đoán WPW. Gia tăng nguy cơ SCD được liên kết với bệnh sử có nhịp tim nhanh triệu chứng, nhiều đường phụ, khoảng R-R kích thích sớm ngắn nhất <250 ms trong AF. Nguy cơ SCD kết hợp với WPW xuất hiện cao nhất trong 2 thập kỷ đầu tiên của đời sống. ^[165-169]

6.1. Điều chỉnh các bệnh nhân có các đường phụ biểu hiện hoặc ẩn

Xem hình 8 cho thuật toán điều trị cấp thời orthodromic AVRT, hình 9 cho thuật toán điều chỉnh tiếp tục orthodromic AVRT và các tư liệu hỗ trợ online 11 đến 15 có tử liệu bổ xung hỗ trợ cho chương 6.

Hình 8, chỉ thuật toán điều chỉnh orthodromic AVRT. Màu sắc tương ứng với Class khuyến cáo ở bảng 1; các thuốc được liệt kê theo alphabê. * Đối với những nhịp được ngừng hoặc tái phát một cách tự nhiên, chuyển nhịp đồng bộ là không phù hợp. AVRT chỉ nhịp nhanh vào lại nhĩ thất; ECG chỉ điện tâm đồ, IV chỉ tiêm truyền tĩnh mạch.

Hình 9 thuật toán điều chỉnh tiếp tục orthodromic AVRT. Màu sắc tương ưng Class khuyến cáo ở bảng 1; các thuốc liệt kê theo alphabe. AVRT chỉ nhịp nhanh vào lại nhĩ  thất; ECG, điện tâm đồ; BN, bệnh nhân, SHD, bệnh tim cấu trúc (gồm bệnh tim thiếu máu cục bộ).

6.1.1. Điều trị cấp thời: Các khuyến cáo (KC 7)

Các khuyến cáo cho điều trị cấp thời Orthodromic AVRT (KC 7)

6.1.2. Điều chỉnh tiếp tục: Các khuyến cáo (KC 8)

Các khuyến cáo cho điều chỉnh tiếp tục Orthodromic AVRT (KC 8)

6.2. Điều chỉnh kích thích sớm không triệu chứng

6.2.1. Các cầu hỏi PICOTS quan trọng

Xem báo cáo ERC tổng quan hệ thống, “Phân tầng nguy cơ đối với biến cố loạn nhịp tim ở bệnh nhân có kích thích sớm không triệu chứng” cho việc xem xét các bằng chứng đầy đủ về việc điều chỉnh kích thích sớm không triệu chứng, 10 và xem dữ liệu trực tuyến bổ sung 13, 14, và 15 cho dữ liệu bổ sung trong kích thích sớm không triệu chứng, được sao chép trực tiếp từ tổng quan hệ thống của ERC. Những khuyến cáo này đã được thiết kế với SR ký hiệu để nhấn mạnh sự chặt chẽ của các hỗ trợ từ tổng quan hệ thống của ERC. Câu hỏi PICOTS 1 đã không cung cấp đủ dữ liệu cho khuyến cáo; các câu hỏi PICOTS 3 khác được đề cập trong các khuyến cáo ở Mục 6.2.2.

Tiếp theo 4 câu hỏi được ERC xem xét:

1.     Độ chính xác của nghiên cứu điện sinh lý (EPs) xâm lấn dự báo tương đối (không triệt phá qua catheter đường phụ) đối lại với không test cho dự báo biến cố rối loạn nhịp (gồm SCD) ở các bệnh nhân kích thích sớm không triệu chứng là gì ?

2.      Tính hữu ích của nghiên cứu EP xâm lấn là gì (không triệt phá qua catheter đường phụ) đối lại với không test để dự báo biến cố rối loạn nhịp (gồm SCD) ở bệnh nhân kích thích sớm không triệu chứng là gì ?

3. Tính hữu ích của nghiên cứu EP xâm lấn (không triệt phá đường phụ qua catheter) hoặc nghiên cứu EP không xâm lấn để dự đoán các biến cố rối loạn nhịp tim (bao gồm SCD) ở bệnh nhân kích thích sớm không triệu chứng là gì ?

4. Hiệu quả và hiệu lực của các nghiên cứu EP xâm lấn với triệt phá qua catheter đường phụ phù hợp so với các test không xâm lấn với điều trị (bao gồm theo dõi) hoặc không có test / triệt phá cho phù hợp để ngăn ngừa các biến cố rối loạn nhịp tim (bao gồm SCD) và cải thiện kết quả ở bệnh nhân kích thích sớm không triệu chứng là gì ?

6.2.2. Các bệnh nhân kích thích sớm không triệu chứng: Các khuyến cáo (KC 9)

Các khuyến cáo cho điều chỉnh các bệnh nhân kích thích sớm không triệu chứng (KC 9 )

6.3. Phân tầng nguy cơ các bệnh nhân có các đường phụ biểu hiện có triệu chứng: Các khuyến cáo (KC 10)

Các khuyến cáo điều chỉnh các bệnh nhân có đường phụ biểu hiện có triệu chứng (KC 10)

(Còn nữa)

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