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đIện tâm đồ
- 1. ĐI N TÂM ĐỆ Ồ BÌNH TH NG VÀ M T S B NH LÝƯỜ Ộ Ố Ệ Đ i t ng: Y4 đa khoaố ượ ThS. Phan Đình Phong B môn Tim m chộ ạ Tr ng ĐHY Hà n iườ ộ
- 2. H TH NG D N TRUY N TIMỆ Ố Ẫ Ề VÀ C S ĐI N SINH LÝ H C C AƠ Ở Ệ Ọ Ủ ĐI N TÂM ĐỆ Ồ
- 3. H TH NG D N TRUY N TIMỆ Ố Ẫ Ề Nút xoang (SA Node) • Là ch nh p t nhiên c a timủ ị ự ủ - 60-100/ ph NÚT XOANG
- 4. NÚT NHĨ TH TẤ Nút xoang (SA Node) Nút nhĩ th tấ (AV Node) • Nh n xung đ ng t nút xoangậ ộ ừ • Truy n xung đ ng xu ng hề ộ ố ệ His - Purkinje • 40-60/ phút n u nút xoangế không phát xung H TH NG D N TRUY N TIMỆ Ố Ẫ Ề
- 5. BÓ HIS Bó His • D n xung đ ng xu ng th tẫ ộ ố ấ • Nh p thoát b n i nhĩ th t:ị ộ ỗ ấ 40-60/phút Nút xoang (SA Node) Nút nhĩ th tấ (AV Node) H TH NG D N TRUY N TIMỆ Ố Ẫ Ề
- 6. Các nhánh bó His M ng Purkinjeạ • D n xung đ ng to ra c th tẫ ộ ả ơ ấ gây kh c cử ự • Nh p thoát:ị 20-40/ phút M NG PURKINJEẠ Nút xoang (SA Node) Nút nhĩ th tấ (AV Node) Bó His H TH NG D N TRUY N TIMỆ Ố Ẫ Ề
- 7. Xung đ ng phát ra t nút xoang…ộ ừ D II
- 8. kh c c nhĩ…ử ự D II
- 9. xung đ ng (b ) tr l i nút nhĩ th t…ộ ị ễ ạ ở ấ D II
- 10. qua các nhánh bó His… D II
- 11. r i to ra m ng Purkinje…ồ ả ạ D II
- 12. kh c c th t…ử ự ấ D II
- 13. Cao nguyên tái c cự D II
- 14. Tái c c nhanh (pha 3)ự D II
- 15. Trình t ho t hoá ĐTĐ bình th ngự ạ ườ
- 16. CÁCH GHI ĐI N TÂM ĐỆ Ồ
- 17. Gi y ghi ĐTĐ tiêu chu nấ ẩGi y ghi ĐTĐ tiêu chu nấ ẩ • V i t c đ gi yớ ố ộ ấ ghi 25 mm/s, M i ô vuông l nỗ ớ t ng ng v iươ ứ ớ 200 ms và m i ôỗ vuông nhỏ t ng ng v iươ ứ ớ 40 ms. • V iớ 10 mm = 1 mV, m i ô vuôngỗ nh ng v iỏ ứ ớ 0.1 mV. 0.1mV0.1mV 0.5mV0.5mV
- 18. 3 chuy n đ o l ng c c chiể ạ ưỡ ự DII = DI + DIII Các chuy n đ o ngo i biênể ạ ạ
- 19. Các chuy n đ o ngo i biênể ạ ạ 3 chuy n đ o đ n c c chi tăng thêmể ạ ơ ự aVR, aVL, aVF
- 20. Các chuy n đ o tr c timể ạ ướ V1, V2, V3, V4, V5, V6
- 21. Các chuy n đ o tr c timể ạ ướ
- 22. 12 chuy n đ o thông d ngể ạ ụ • 6 chuy n đ o ngo i biên “nhìn” dòng đi n timể ạ ạ ệ trên m t ph ng trán.ặ ẳ • 6 chuy n đ o tr c tim “nhìn” dòng đi n timể ạ ướ ệ trên m t ph ng ngang.ặ ẳ
- 23. Nguyên t c âm - d ngắ ươ • M i chuy n đ o đ u có m t đi n c c âm và m tỗ ể ạ ề ộ ệ ự ộ đi n c c d ng.ệ ự ươ • M t dòng đi n tim h ng t c c âm t i c c d ngộ ệ ướ ừ ự ớ ự ươ c a chuy n đ o nào s d ng trên chuy n đ o đóủ ể ạ ẽ ươ ể ạ
- 24. CÁCH Đ C ĐI N TÂM ĐỌ Ệ Ồ
- 25. Các tiêu chu n c a nh p xoang:ẩ ủ ị • Nhìn th y sóng P t i thi u 1 trong 12 CĐấ ố ể • Sóng P đ ng tr c m i ph c b QRSứ ướ ỗ ứ ộ • Kho ng PQ (PR) trong gi i h n bìnhả ớ ạ th ngườ • Sóng P d ng D1, D2, aVF, V5, V6 vàươ ở âm aVRở • Kho ng các gi a các sóng P đ u, t n sả ữ ề ầ ố t 60 – 100/phútừ Xác đ nh nh p xoang hay không?ị ị
- 26. • Đo b ng th c đo đi n timằ ướ ệ • Ho c tính theo công th c:ặ ứ T n s tim = 60/ kho ng RRầ ố ả (tính b ng giây)ằ Xác đ nh t n s timị ầ ố
- 27. Xác đ nh tr c đi n timị ụ ệ • Tính góc ∝ • c l ngƯớ ượ d a vào hìnhự d ng R, Sạ ở D1 và aVF
- 28. Xác đ nh tr c đi n timị ụ ệ • QRS D1: d ngở ươ • QRS aVF: d ngở ươ tr c trung gianụ
- 29. DÀY TH T, DÀY NHĨẤ
- 30. Dày nhĩ ph iả
- 31. Dày nhĩ trái
- 32. Dày th t ph iấ ả
- 33. Dày th t ph iấ ả
- 34. Dày th t ph iấ ả
- 35. Dày th t tráiấ
- 36. Dày th t tráiấ
- 37. Dày th t tráiấ
- 38. B NH M CH VÀNHỆ Ạ
- 39. • Thi u máuế D i n i tâm m c: T d ng cao, nh n, đ i x ngướ ộ ạ ươ ọ ố ứ D i th ng tâm m c: T âm sâu, đ i x ngướ ượ ạ ố ứ • T n th ngổ ươ D i n i tâm m c: ST chênh xu ngướ ộ ạ ố D i th ng tâm m c: ST chênh lênướ ượ ạ • Ho i tạ ử Sóng Q b nh lý (sâu, r ng)ệ ộ ĐTĐ trong b nh m ch vànhệ ạ
- 40. Nh i máu c timồ ơ
- 41. Nh i máu c tim c pồ ơ ấ
- 42. Nh i máu c tim c pồ ơ ấ
- 43. Thi u máu c tim d i th ng tâm m cế ơ ướ ượ ạ
- 44. Ho i t c timạ ử ơ
- 45. R I LO N NH P TIMỐ Ạ Ị
- 46. Nh p ch mị ậ R I LO N NH P TIMỐ Ạ Ị
- 47. • Nút xoang phát xung nh ng quá ch mư ậ Nh p ch m xoangị ậ
- 48. • Nút xoang không phát xung đ ngộ • Không th y kh c c nhĩ trên ĐTĐấ ử ự • Vô tâm thu Ng ng xoangư
- 49. • Xen k các giai đo n nh p nhanh vàẽ ạ ị ch m t nút xoang ho c tâm nhĩ.ậ ừ ặ • Ch m < 60 ck/phậ • Nhanh >100 ck/ph H i ch ng nh p nhanh-ch mộ ứ ị ậ
- 50. • Bl c thoáng qua các xung đ ng t nút xoangố ộ ừ • Xác đ nh b ng t ng quan gi aị ằ ươ ữ các kho ng P-Pả Bl c xoang nhĩố
- 51. Bl c nhĩ th t c p Iố ấ ấ • Kho ng PR > 200 msả • Do ch m tr d n truy n qua nút nhĩ th tậ ễ ẫ ề ấ
- 52. • Kho ng PR dài d n ra cho đ n khi m t sóng P bả ầ ế ộ ị bl c không d n đ c xu ng th t.ố ẫ ượ ố ấ Chu kỳ Wenckebach Bl c nhĩ th t c p 2 - Mobitz Iố ấ ấ
- 53. • Các kho ng PP v n đ u và có nh ng nhát bóp nhĩ (P)ả ẫ ề ữ không d n đ c xu ng th tẫ ượ ố ấ – Ví d : Bl c 2:1 (2 P đi v i 1 QRS)ụ ố ớ Bl c nhĩ th t c p 2 - Mobitz 2ố ấ ấ
- 54. • Xung đ ng t nhĩ không d n xu ng đ c th tộ ừ ẫ ố ượ ấ – Nh p th t = 37 ck/phị ấ – Nh p nhĩ = 130 ck/phị – Kho ng PR thay đ i, không còn liên h gi a P và Rả ổ ệ ữ Bl c nhĩ th t c p 3ố ấ ấ
- 55. Tóm t tắ R i lo n t o xungố ạ ạR i lo n t o xungố ạ ạ R i lo n d n xungố ạ ẫR i lo n d n xungố ạ ẫ Phân lo i nh p ch mạ ị ậ • HC nh p nhanh/ch mị ậ • Nh p ch m xoangị ậ • Ng ng xoangư • Bl c nhĩ th t c p 3ố ấ ấ • Bl c nhĩ th t c p 2ố ấ ấ • Bl c nhĩ th t c p 1ố ấ ấ • Bl c xoang nhĩố
- 56. Nh p nhanhị R I LO N NH P TIMỐ Ạ Ị
- 57. Nh p nhanh xoangị • Ngu n g c:ồ ố Nút xoang • T n s :ầ ố 100-180 ck/ph • C ch :ơ ế Tăng tính t đ ngự ộ
- 58. Nh p nhanh nhĩị • Ngu n g c:ồ ố ngo i v tâm nhĩổ ạ ị • T n s :ầ ố >100 ck/ph • C ch :ơ ế Tăng tính t đ ngự ộ
- 59. Ngo i tâm thuạ Ngo i tâm thu nhĩ (PAC)ạ • Ngu n g c:ồ ố Tâm nhĩ (ngoài vùng nút xoang) • C ch :ơ ế B t th ng tính t đ ngấ ườ ự ộ • Đ c đi m:ặ ể Sóng P b t th ng đ n s m, theo sauấ ườ ế ớ b i ph c b QRS gi ng nh nh p c sở ứ ộ ố ư ị ơ ở
- 60. Ngo i tâm thu th t (PVC)ạ ấ • Ngu n g c:ồ ố Tâm th tấ • C ch :ơ ế B t th ng tính t đ ng, vào l iấ ườ ự ộ ạ • Đ c đi m:ặ ể Ph c b QRS đ n s m, giãn r ng,ứ ộ ế ớ ộ theo sau b i m t kho ng ngh bùở ộ ả ỉ Ngo i tâm thuạ
- 61. Ngo i tâm thu th tạ ấ •Nh p đôiị (Bigeminy) •Nh p baị (Trigeminy) •Nh p b nị ố (Quadrigeminy)
- 62. • Ngu n g c:ồ ố Nhi u ngo i v tâm th tề ổ ạ ị ấ • C ch :ơ ế B t th ng tính t đ ngấ ườ ự ộ • Đ c đi m:ặ ể Các nhát ngo i tâm thu có kho ngạ ả ghép, hình d ng và tr c khác nhauạ ụ Ngo i tâm thu th t đaạ ấ ổ
- 63. Cu ng nhĩồ • Ngu n g c:ồ ố Nhĩ trái ho c nhĩ ph iặ ả • C ch :ơ ế Vào l iạ • Đ c đi m:ặ ể Sóng F, đáp ng th t 2/1, 4/1ứ ấ
- 64. Rung nhĩ • Ngu n g c:ồ ố Nhĩ ph i và/ ho c nhĩ tráiả ặ • C ch :ơ ế Nhi u vòng vào l i nhề ạ ỏ • T n s :ầ ố 400 ck/ph • Đ c đi m:ặ ể Sóng f, t n s th t không đ uầ ố ấ ề
- 65. Tim nhanh k ch phát trên th tị ấ • C ch :ơ ế Vòng vào l iạ • T n s :ầ ố 140 - 240 ck/ph • Đ c đi m:ặ ể QRS thanh m nh, t n s tim r t đ u.ả ầ ố ấ ề
- 66. • Ngu n g c:ồ ố Tâm th t (m t ngo i v )ấ ộ ổ ạ ị • C ch :ơ ế Vào l i, b t th ng tính t đ ng,ạ ấ ườ ự ộ ho t đ ng cò n yạ ộ ẩ • Đ c đi m:ặ ể QRS giãn r ng và ch có m t d ngộ ỉ ộ ạ Tim nhanh th t đ n d ngấ ơ ạ
- 67. • Ngu n g c:ồ ố Tâm th t (nhi u ngo i v )ấ ề ổ ạ ị • C ch :ơ ế Vào l i, b t th ng tính t đ ng,ạ ấ ườ ự ộ ho t đ ng cò n yạ ộ ẩ • Đ c đi m:ặ ể QRS giãn r ng, nhi u hình d ngộ ề ạ khác nhau Tim nhanh th t đaấ ổ
- 68. • Ngu n g c:ồ ố Tâm th tấ • C ch :ơ ế Vào l i, ho t đ ng cò n yạ ạ ộ ẩ • T n s :ầ ố 200 – 250 ck/ph • Đ c đi m:ặ ể QRS bi n d ng, xoay quanh m t tr cế ạ ộ ụ Xo n đ nh - Torsades de Pointesắ ỉ
- 69. • Ngu n g c:ồ ố Tâm th tấ • C ch :ơ ế Nhi u vòng vào l i nhề ạ ỏ • Đ c đi m:ặ ể Không còn ph c b QRS thayứ ộ b ng nh ng sóng th t ng u nhiênằ ữ ấ ẫ Rung th t (VF)ấ
- 70. Phân lo i nh p nhanhạ ị Tóm t tắ R i lo n t o xungố ạ ạR i lo n t o xungố ạ ạ R i lo n d n xungố ạ ẫR i lo n d n xungố ạ ẫ • Nh p b n i gia t cị ộ ố ố • Ngo i tâm thuạ • Nh p nhanh nhĩị • Nh p nhanh xoangị • Nh p t th t gia t cị ự ấ ố • Rung nhĩ • Cu ng nhĩồ • Tim nhanh trên th tấ • Tim nhanh th tấ • Rung th tấ
- 71. ÔN T PẬ
- 76. Chan doan la rung nhi • Vi co song p lan tan • Tren dien tam do con thay phuc bo qrs thay doi :am manh o v1 va co dang RS o v5.
- 78. Chan doan la rung nhi • Vi song p lan tan • Ko phai la 1 mat nhip xoang vi ko co ngi bu
- 80. Chan doan la ngoai tam thu that • Vi co song qrs bien dang dien hinh • Nhip xoang • Tan so bt • Tuy duong dang dien co ve hoi cong nhung ko co van de gi
- 82. • Day la nhip nhanh tren that • Vi ro rang la co nhip nhanh • Va ko co song P
- 84. • Theo minh thi day la mot cuong that • Vi cac song rat deu dan nhung ko co song P • Co mot hinh anh hoi nghi ngo la hinh co moc nhung ro rang ko the la 1 block nhanh duoc,vi neu la block nhanh thi phai :nhip xoang, song qrs rat dien hinh
- 86. Chan doan :block nhanh phai • vi: co thoi gian qrs dai • Co nhanh noi dien dai • Qrs co dang 2 dinh (hay co moc) • Ko phai la day that vi xem o v1 va v5 thi ko co cac hinh anh dien hinh cua day that phai va trai
- 89. Nhip cham.kem theo block nhanh • Ko ro block nhanh nao
- 91. Chan doan la 1 block cap2 mobit 2-1 co kem theo mot block nhanh phai • Block cap 2 vi thay co 2 song p doc lap voi 1 qrs • Co block nhanh phai vi co dang qrs co dang 2 dinh o v2 :rSR.tuy nhien chua chac chan vi :chua rong lam. O v5 chua co dang dien hinh RS
Hinweis der Redaktion
- We use the term Conduction System to describe the electrical pathway of an electrical impulse that causes a heart beat.
- The Conduction System in a normal heart is begins with the Sinus Node or SA Node. The Sinus Node (SA Node): Located in the upper right atrium Known as the heart’s ‘Natural Pacemaker’ Produces resting rates between 60-100 BPM The SA Node has ‘automaticity’, which will be discussed later in this Module. It’s rate of automaticity is normally faster than all other parts of the heart, and therefore, dictates the rate at which the heart beats. This is known as “Sinus Rate”.
- The Atrioventricular Node or AV Node: Located between the Atrium and the Ventricles in the interatrial septum close to the tricuspid valve Receives the impulse from the SA Node and delivers it through the Bundle of His (the forefront of the His-Purkinje network) Produces rates at 40-60 BPM if the SA Node fails to fire Conduction through the AV Node is slow, allowing appropriate fill time for the ventricles prior to ventricular contraction. If the SA Node fails to deliver an impulse to the AV Node, the AV Junctional Tissue will deliver an impulse to the Bundle of His at rates between 40-60 BPM.
- Bundle of His: Together with the AV Node make up the AV Junctional Tissue Begins conduction to the ventricles Junctional tissue produces rates between 40-60 BPM
- Bundle Branches & Purkinje Fibers (make up the Purkinje Network): Distribute the electrical impulse to the cardiac muscle allowing for depolarization (contraction) of the ventricle Together with the Purkinje Fibers make up the Ventricular Conduction System Can deliver impulses at rates between 20-40 BPM, known as an ‘escape’ rhythm
- Initiation of the cardiac cycle normally begins with initiation of the impulse at the SA (sinoatrial) node.
- After the SA node fires, the resulting depolarization wave passes through the right and left atria, which produces the P-wave on the surface EKG and stimulates atrial contraction.
- Following activation of the atria, the impulse proceeds to the atrioventricular (AV) node, which is the only normal conduction pathway between the atria and the ventricles. The AV node slows impulse conduction, which allows time for the atria to contract and for blood to be pumped from the atria to the ventricles prior to ventricular contraction. Conduction time through the AV node accounts for most of the duration of the PR interval. Just below the AV node, the impulse passes through the bundle of His. A small portion of the last part of the PR interval is represented by the conduction time through the bundle of His.
- After the impulse passes through the bundle of His, it proceeds through the left and right bundle branches. A small portion of the last part of the PR interval is represented by the conduction time through the bundle branches.
- Next the impulse passes through the Purkinje fibers (interlacing fibers of modified cardiac muscle). Conduction time through the Purkinje system is represented by a small portion of the last part of the PR interval.
- The impulse passes quickly through the bundle of His, the left and right bundle branches, and the Purkinje fibers, leading to depolarization and contraction of the ventricles. The QRS complex on the EKG represents the depolarization of the ventricular muscle mass.
- The Plateau Phase lasts up to several hundred milliseconds.
- Repolarization of the ventricles generates a current in the body fluids and produces a T-wave. This takes place slowly, and generates a wide wave.
- Here is another graphical view with each EKG wave represented with respect to the heart function associated with it.
- An EKG not only reveals heart beat activity, but it also reflects heart rate. The rate of the waves is measured by the small squares on an EKG. Each small square represents 40 milliseconds in time. To make time measurements easier, the small squares are grouped into intervals of 5 that make up a large, bold square measuring at 200 milliseconds. To measure heart rate, the count of boxes from the peak of one R-wave to the peak of the next R-wave is taken, then converted to beats per minute. For example, if the measurement between two R-wave peaks equals 1,000 milliseconds, the heart rate converts to 60 beats per minute.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Different areas of the normal heart have differing rates of automaticity. The fastest pacemaker cells will drive the heart rate. In a normal heart, the SA node is the fastest, and therefore acts as the primary pacemaker that drives the rate. A normal resting heart rate ranges between 60-100 BPM. The faster rate of the SA node activates the depolarization mechanism in other cells. Consequently, the impulse formation abilities of other pacemaker cells are suppressed and not used. If the SA node fails to fire, the AV node generally takes the lead, beating at a rate of 40 to 60 beats per minute. If the AV node also fails to fire, the ventricular cells then have the ability to take over the rhythm, beating at a much slower rate of 20 to 40 BPM. This is often referred to as the “escape rhythm.” There is no pre-determined ventricular cell that initiates a pulse. The initiating pulse can come from any cell within the ventricle, including the Purkinje network.
- Sinus bradycardia occurs when the SA node fires at an abnormally slow rate.
- Sinus Arrest occurs when there is a pause in the rate at which the SA node fires. With sinus arrest, there is no relationship between the pause and the basic cycle length.
- Brady/Tachy syndrome occurs when the SA node has alternating periods of firing too slowly (&lt; 60 BPM) and too fast (&gt;100 BPM). Brady/Tachy syndrome often manifests itself in periods of atrial tachycardia, flutter, or fibrillation. Cessation of the tachycardia is often followed by long pauses from the SA node.
- SA exit block occurs when the SA node fires, but the impulse does not conduct to the pathways that cause the atrium to contract. In SA exit block there is a relationship between the pattern and the basic cycle length (because the sinus node continues to fire regularly), of approximately two, but less commonly three or four times the normal P-P interval.
- AV block can be described as a prolongation of the PR interval, the interval from the onset of the P-wave to the onset of the QRS complex. First-degree AV block is defined by a PR interval greater than 0.20 seconds (200 ms). First-degree AV block can be thought of as a delay in AV conduction, but each atrial signal is conducted to the ventricles (1:1 ratio).
- Second-Degree AV block is characterized by intermittent failure of atrial depolarizations to reach the ventricle. There are two patterns of second-degree AV block. Type I is marked by progressive prolongation of the PR interval in cycles preceding a dropped beat. This is also referred to as Wenckebach or Mobitz Type I block. The AV node is most commonly the site of Mobitz I block. The QRS duration is usually normal.
- Mobitz Type II Second-Degree AV block refers to intermittent dropped beats preceded by constant PR intervals. To differentiate Mobitz I from Mobitz II, note the PR interval in the beats preceding and following the dropped beat. If a difference between these two PR intervals is more than 0.02 seconds (20 ms), then it is Mobitz I. If the difference is less than 0.02 seconds, then it is Mobitz II. The infranodal (His bundle) tissue is most commonly the site of Mobitz II block. *Note: Advanced second-degree block refers to the block of two or more consecutive P-waves (i.e., 3:1 block).
- Third-Degree AV block is also referred to as complete heart block. It is characterized by a complete dissociation between P-waves and QRS complexes. The QRS complexes are not caused by conduction of the P-waves through the AV node to the ventricles. In Third-Degree AV block, the QRS is initiated at a site below the AV node (such as in the His bundle or the Purkinje fibers). This “escape rhythm” is normally 40–60 BPM if initiated by the His bundle (a junctional rhythm) and &lt;40 BPM if initiated by the Purkinje fibers.
- To review: Bradyarrhythmias can be classified according to the underlying cause of the disorder - impulse formation or impulse conduction. Impulse generation disorders include sinus bradycardia, sinus arrest (or sinus pause), and brady/tachy syndrome. Impulse conduction disorders include exit block, AV block and Bifascicular/Trifascicular block.
- Now, let’s review tachyarrhythmias.
- In Sinus Tachycardia, the EKG deflection will show a normal P and R-wave depolarization, with a rapid tachycardic rate Sinus Tachycardia rates range between 100-180 BPM The underlying Mechanism for Sinus Tachycardia is Abnormal Automaticity (Hyper-Automaticity)
- Atrial Tachycardia is defined as a series of 3 more consecutive atrial premature beats occurring at a rate of &gt;100 BPM. Atrial tachycardia is usually paroxysmal (PAT – Paroxysmal atrial tachycardia), it starts and ends abruptly. It can occur in healthy as well as diseased hearts and may result from emotional stress or excessive use of alcohol, tobacco, or caffeine. Origin: Ectopic focus located in the atrium Mechanism: Abnormal Automaticity
- PACs originate in parts of the atrium other than the sinus node. These impulses occur before the sinus node depolarizes. They are conducted through the atrium and slow down, just like a normal sinus beat, when they reach the A-V node. They are conducted through the ventricle in the same fashion as a normal sinus beat. PACs are very common, and can be completely unknown to the person. Sometimes they are perceived as a &quot;skip&quot; or a &quot;pause.&quot;
- Premature ventricular contractions (PVCs) are also extremely common. These originate in the ventricle, and are sometimes perceived by patients as palpitations. Multiple, consecutive PVCs can trigger ventricular tachycardia. However, the vast majority are benign, and do not require treatment. PVCs are recognized by a broad, wide complex occurring earlier than a sinus beat would have been expected and is followed by a full compensatory pause (when the distance between the beats before and after the PVC equals twice the normal cycle length).
- Ventricular Premature beats that form patterns are classified according to the number of normal ventricular beats that occur between premature beats. Bigeminy – PVC every other beat; – PVC every third beat; or - PVC every fourth beat.
- Not every premature beat is alike. This is an example of a variety of PVCs you may see.
- Atrial flutter produces an atrial rate between 250 and 400 BPM. The ventricular rate may increase, but it is always slower than the atrial rate. During atrial flutter, atrial impulses are conducted to the ventricles in various ratios. Even conduction ratios (2:1, 4:1) are more common than odd ratios (3:1, 5:1). In a 2:1 ratio, there are two flutter waves for every QRS complex. A constant conduction ratio (e.g., 2:1) results in a regular ventricular rhythm (most common). A variable ratio (e.g., 4:1 to 2:1 to 5:1) results in an irregular ventricular rhythm.
- Atrial Fibrillation (AF) is characterized by random, chaotic contractions of the atrial myocardium. Patients have an atrial rate of 400 BPM or more, often too fast to measure on an EKG. A surface EKG shows atrial fibrillation as irregular, wavy deflections (fibrillatory waves) between narrow QRS complexes. The fibrillatory waves vary in shape, amplitude, and direction. The chaotic nature of atrial fibrillation results in a grossly irregular ventricular rhythm. The rhythm is considered controlled if the ventricular rate is less than 100 BPM; uncontrolled if the ventricular rate conducts to greater than 100 BPM. Mechanism: In AF, the multiple wavelets of reentry do not allow the atria to organize. The ectopic focus or foci are said to be located around or within the pulmonary veins. Drugs such as flecainide, sotalol and amiodarone can terminate and prevent atrial fibrillation. Drug therapy can be used before or after DC cardioversion to maintain sinus rhythm after cardioversion.
- This is a reentrant supraventricular rhythm whose reentry circuit is located in the region of the atrioventricular node. It is characterized by a QRS morphology that is normal for the patient. The rate of AVNRT is commonly between 150-230 BPM, and can exceed 250 BPM in teenagers. Note that on the EKG, P-waves are unseen and are usually buried in the QRS. Approximately 60% of narrow-complex tachycardias are found to be caused by AVNRT. Here are some other characteristics of AVNRT: A paroxysmal onset and termination is seen with AVNRT. There is both a typical and atypical form of AVNRT. Typical AVNRT is a result of a shift in conduction from the fast to the slow pathway, and is seen in 90% of the patients with AVNRT. Atypical AVNRT is a result of a conduction shift from the slow to fast or slow to the slow pathway. The atypical form is less common, occurring in 10% of the patients with AVNRT. AVNRT is not associated with underlying heart disease. It may present at any age, but usually occurs in the mid 40s, and may be more frequent in females. AVNRT appears to be catecholamine sensitive, as there are increased episodes reported with exercise, emotional stress, and use of caffeine. The frequency of AVNRT episodes can be from once every 2 or 3 years to several times a day.
- Monomorphic morphology indicates that electrical activity has a single point of origin or focus. Monomorphic VT is usually initiated by a PVC and sustained by reentry of a single loop. Here, we can see the EKG characteristics that help define VTs: Rapid, wide, and regular QRS complexes Rate of 120 BPM or greater Uniform beat-to-beat appearance The T-waves are large with deflections opposite the QRS complexes P-waves are usually not visible, therefore the PR interval is not measurable
- The QT or repolarization syndrome are typically associated with polymorphic VT are often called “torsades de pointes” due to original French description of the QRS complexes as “twisting” about its axis. Polymorphic VT morphology has a single focus that nonetheless wanders through a number of different points of origin. EKG characteristics are: Broad (wide) QRS’s, Usually at rates of 120 BPM or greater (500 ms or less) Highly irregular QRS wave Variable beat-to-beat appearance
- Torsades de Pointes (TdP – twists of points) is a distinctive VT in which the QRS complexes change in morphology from positive to negative and appear to twist around an imaginary base line. The changing patterns are due to a movement in the reentrant mechanism. TdP is associated with prolonged repolarization, may be acquired or congenital and may be a very deadly form of VT. Events leading to TdP are: Hypokalemia Prolongation of the action potential duration Early afterdepolarizations Critically slow conduction that contributes to reentry
- The following EKG findings help electrophysiologists to diagnose VF: P-waves and QRS complexes are not present Heart rhythm is highly irregular The heart rate is not defined (without QRS complexes) While multiple wavelets of reentry maintain VF, there is some belief that focal activation initiates it.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.
- Now, let’s review tachyarrhythmias.