Curs ECG

ELECTROCARDIOGRAMA NORMAL
ELECTROCARDIOGRAMA
1) Definiie 2) Istoric
3) Principiu
4) Electrozi i derivaii 5) Analiza ECG
ELECTROCARDIOGRAMA
3) Principiu
DEFINIIE
Rezultatul modificrilor electrice care activeaz contracia atriilor i ventriculilor
Reprezint nregistrarea la suprafaa corpului a variaiilor de potenial ale cmpului electric cardiac, produse de depolarizarea i repolarizarea celulelor miocardice
ELECTROCARDIOGRAMA
1. Definiie 2. Istoric 3. Principiu 4. Electrozi i derivaii 5. Convenii n electrocardiografie 6. Electrogeneza undelor ECG 7. Analiza ECG
ISTORIC
1791 Galvani a emis teoria electricitii animale 1792 Volta electricitatea se datoreaz coninutului organismelor n metale i diferena de concentraie a acestora genereaz curentul electric
Entuziasm folosirea curentului electric pentru reanimarea unor decedai (studii pe criminali spnzurai)
ISTORIC
1887 Fiziologul britanic Augustus D. Waller din Londra a publicat primele studii de electrocardiografie uman, realizate cu un electrometru capilar 1889 Fiziologul olandez Willem Einthoven l-a vzut pe Waller demonstrndu-i experimentul cu ocazia Primului Congres al Fiziologilor din Bale. Jimmy 1890 GJ Burch din Oxford a imaginat un dispozitiv de corectare a oscilaiilor electrometrului 1893 Willem Einthoven introduce termenul de electrocardiogram la ntrunirea Asociaiei Medicale Olandeze
ISTORIC
1901
Einthoven inventeaz un nou dispozitiv pentru nregistrarea EKG, din electrozi din argint
1924
Willem Einthoven ctig premiul Nobel pentru inventarea electrocardiografului
Heart
Conducerea impulsului electric n inim

Este realizat de ctre esutul nodal al inimii format din:
Nodul sino-atrial
Nodul atrio-ventricular
Fasciculul Hiss Reeaua Purkinje

Nodul sino-atrial este format dintr-un grup de celule specializate, cu proprietatea de a descrca automat impulsuri electrice (principalul pacemaker al inimii) aflat la nivelul atriului drept

Mai multe ci internodale fac legtura ntre NSA i nodul atrioventricular (NAV)

Aceste fibre se continu apoi spre apex unde se mpart n mai multe fibre Purkinje mici care se distribuie celulelor contractile ventriculare
PRINCIPIU
Inima poate fi considerat o baterie, un generator de curent electric inclus ntr-un volum conductor (corp) Inima genereaz un cmp electric ce poate fi evideniat la suprafaa corpului, prin electrozi plasai pe tegument
PRINCIPIU
Depolarizare i Repolarizare
n repaus, cardiomiocitele sunt ncrcate pozitiv pe versantul extern al membranei i negativ la interior n timpul depolarizrii, potenialul de membran se inverseaz. Negativitatea de repaus a interiorului se reduce spre 0 i apoi interiorul devine pozitiv ca urmare a influxului de Na+.
Potenialul de aciune
Classification of Electrocardiogram (ECG) Waveforms for the Detection of Cardiac Problems
NORMAL ECG
Pozitionare electrozi periferici
right
left
Derivaiile unipolare ale membrelor

aVL
perpendicular pe DII culege diferena de potenial dintre L (electrodul pozitiv) i R i F legai mpreun (electrodul negativ)
Derivaiile standard ale membrelor
DI
electrodul + e plasat pe membrul superior stng electrodul e plasat pe membrul superior drept
DII
electrodul e plasat pe membrul superior drept electrodul + e plasat pe membrul inferior stng
DIII electrodul e plasat pe membrul superior stng electrodul + e plasat pe membrul inferior stng
aVR, aVL i aVF exploreaz planul frontal al inimii electrodul explorator (pozitiv) se plaseaz pe R, L sau F, iar ceilali doi electrozi se leag mpreun, reprezentnd electrodul de referin (negativ)

aVR
perpendicular pe DIII culege diferena de potenial dintre R (electrodul pozitiv) i L i F legai mpreun (electrodul negativ)

aVF perpendicular pe DI culege diferena de potenial dintre F (electrodul pozitiv) i R i L legai mpreun (electrodul negativ)
Triunghiul lui Einthoven
Derivaiile unipolare precordiale
TRIANGULO DE EINTHOVEN
Standardizarea ECG
implic:
pe vertical:
1mm = 0,1mV, permind aprecierea amplitudinii undelor
pe orizontal:
1mm = 0,04 secunde (la viteza de 25 mm/sec), permind aprecierea duratei undelor i intervalelor
ONDA P
ONDA R
ONDA T
ONDA Q
ONDA S
Se debe medir la duracin y voltaje de los complejos y ondas
Valores normales de voltaje y duracin
Duracin: 0,08 a 0,10 s (< 0,12 s o < 2,5 mm) Altura: < de 0,25 mV (< 2,5 mm)
Onda P
ECG waveform
The QRS complex corresponds to depolarization of ventricles Need Matlab and Fourier Analysis to develop algorithm for QRS
Intervalo PR
Incluye tiempo de despolarizacin auricular y de conduccin auriculoventricular y del sistema His- Purkinje
Intervalo PR
Se mide desde el inicio de la onda P hasta el inicio del complejo QRS. Duracin: desde inicio de la P al inicio del QRS, va de 0,12 a 0,20 seg

Complejo QRS:
despolarizacin ventricular. Duracin:
0,06 a 0,10 segundos
QRS: presenta diversas morfologas en diferentes derivaciones

QRS:
1 onda negativa : onda Q. 1 onda positiva : onda R. onda negativa que sigue : onda S.

QRS: .
Se utilizan maysculas o minsculas en funcin del tamao de dichas ondas. Cuando hay una sola onda negativa se denomina complejo QS
QRS
deflexin intrinsecoide: tiempo desde el inicio del QRS hasta el momento en que la onda R cambia de direccin. duracin normal <0,045 seg.
se utiliza en el diagnstico de la hipertrofia ventricular izquierda, en la dilatacin ventricular izquierda y en el hemibloqueo anterior

Segmento ST:
periodo isoelctrico que sigue al QRS.

Va desde el punto J (punto de unin del segmento ST con el QRS ) hasta el inicio de la T
Segmento ST
Tiempo entre la despolarizacin total del ventrculo y su repolarizacin
Mide 0,12 segundos o menos
Segmento ST
En la mayora de las derivaciones es plano
Debe estar al mismo nivel que el segmento TP que sigue.
Segmento ST
Ascenso o depresin del ST: sugerente de isquemia miocrdica
Segmento ST
Entre V1 y V3 presenta rpido ascenso y se fusiona con onda T difcil de identificar.
Onda T: onda asimtrica, cuya 1

mitad es una curva ms gradual que
la 2. Su orientacin coincide con la del QRS.
Onda T
representa la repolarizacin y reposo ventricular (periodo refractario) Dura aproximadamente 0,20 segundos o menos y mide 0,5 mV
Onda T
Inicio onda T : periodo refractario efectivo Se altera en una serie de patologas (HVI, infarto miocardio, alteracin cido base, hiperkalemia)
Analiza unda U
acelasi sens cu unda T vizualizare optima V3 evidentiere:- hK+, cu polaritate nemodif. - ischemie, incarc. VS din HTA, IMi, IAo neg - ECG de repaus, U neg. stenoza TC sau IV

Intervalo QT:
desde inicio de QRS hasta fin de onda T. De 0,2 a 0,4 segundos. Aproximadamente 40% del R-R.
Intervalo Q-T
Representa toda la actividad ventricular.
Depende da la frecuencia cardiaca: a mayor frecuencia, menor QT (repolarizacin se acorta) Se prolonga con la edad y algunos frmacos
INTERVALOS
120-200 mseg
80-100 mseg 350-440 mseg
Fibrilatie atriala
Bradicardie sinusala
Rotatie orara
Rotatie antiorara
SAS
SAD
asocierea la HVS a HAS este uzuala, inclusa in crit. dg. ECG nu diferent. HVS concentr. de dilat. VS. marire de VS ECG nu este de cele mai multe ori sufic. Pt. caract.marirea d formule de expunere: 1) HVS = crit. dg. clare 2) elem. de HVS = unele crit., dar nu majorit. 3) posibil HVS = prea putine criterii, cu specificit.
HVS
Strain
Suprasolicitarea de VD
mecanism compensator, in final maladaptativ, de lunga dura aparut ca urmare a solicitarilor de volum si de presiune impuse miocardului VD etiologie: incarcare de volum - DSV, Fallot, PCA (sunt stg. d incarcare de presiune HTP esent., HTP sec.(emfi TBC, bronsiectazii bilat., fibroze pulm., SM fiziopatol.- balanta vectoriala VD-VS se schimba pana la pred VD, in cazuri extreme de HVD - inversarea asp. normal pe ECG: R in V1, V2 + S in V5, V6 - rotatie orara, catre anterior a VD + rotatie posterio a vf. inimii - prin masa VD asincronism VD-VS
consecinte ECG: - devierea ax. dreapta QRS - modif. modele epicard. HVD moderat - hvoltaj QRS - nemodif. TADI HVD avansata - asincronism inversat = Hdeviatie dr. = invers. modele epicar
HVD concentric - Htrof. masa septala dr. QS V5, V6, aVL, - tulb. sec. faza term imag. dir. V1,V2, imag indir. V5, V6, D1, aV difera asp. electrofiziol. intre HVD de orig. volemica (parietala cea presionala (rezistenta, concentrica) in HVD volemica se asoc. un grad de dilat. VD
Criterii simplificate: 1) deviatie axiala > 900 2) R V1 > 7 mm 3) R V1 + S V5/V6 > 10 mm 4) R/S V1 >1 5) S/R V6 >1 6) TADI V1 > 0.035 sec. 7) aspect de BRD 8) ST T strain D2, D3, aVF 9) P pulmonar / P congenital 10) Aspect S1S2S3 la copii spre deoseb. de HVS, aici asp. complet de HVD este rar HVD se pot insoti si de dilat. AD, cu asp. de SAD in caz de SMi, cu apar. de P mitral asociat dg. diferential: a) sdr. WPW unda d b) BRD masurare de TADI c) IMA postero-bazal si posterolatera strain: asociaza tulbur. independente celor strict de HVD
Supraincarcre de VS + VD
Criteriile ECG: Criterii de voltaj pt HVS in precordiale + Hdeviatie ax spre Criterii de voltaj pt HVS + R V1, V2 S putin adanc V1 + S mai adanc V2 SAS ca expresie a HVS + oricare din: S/R >1 V5,V6 S > 7 mm V5, V6 deviere ax. dr.
HVD
Strain
ECG Waveform
Electrical signal spreads from the right atrium to the left atrium, this is a P wave on the diagram. This has been known to show atrium enlargement
T Wave
The T wave represents the recovery of the ventricles Inverted T wave can be a sign of coronary problems
Goals
3-Nov-08
Have Matlab extracting ECG waveform, develop a algorithm to detect the QRS complex
24-Nov-08
Have Implement a neural network and integrate with the Front End Processor. Verity using the MIT-BIH database
12-Jan-09
Transfer the ECG system from Matlab to C, as a real-time Implementation. The neural network needs to be in C.
Goals
9-Feb-09
Develop hardware circuit to interact with the software, thus a circuit that has a ECG sensor
9-Mar-09
Investigate possible extensions of the system. Eg. Web-based database system that could be used story cardiology records and analysis
Health and Safety

Design of electronic circuits Hardware/software conflicts Testing of human subjects need approval
DESPOLARIZACION VENTRICULAR
El proceso de la despolarizacin ventricular esta representado en EKG por el complejo QRS, que es la suma de una secuencia de vectores instantneos.
VECTORES QRS
DERECHA- ADELANTE ARRIBA - ATRS
IZQUIERDA - ATRS
REPOLARIZACION VENTRICULAR
La repolarizacion ocurre en direccin opuesta al vector QRS, va desde el epicardio hacia el endocardio.
ELECTROCARDIOGRAMA
3) Principiu
ELECTROZI I DERIVAII
O derivaie este format din doi electrozi care culeg variaiile de potenial electric produse n cursul ciclului cardiac
1. BIPOLARE
Derivaiile standard ale membrelor: DI, DII, DIII
2. UNIPOLARE
Derivaiile unipolare ale membrelor: aVR, aVL, aVF Derivaiile unipolare precordiale:V1-V6

DI, DII i DIII descrise de Einthoven nregistreaz direcia, amplitudinea i durata variailor de voltaj n plan frontal Rezult prin combinarea a trei electrozi:
R (plasat pe braul drept) L (plasat pe braul stng) F (plasat pe gamba stng)

aVR
perpendicular pe DIII culege diferena de potenial dintre R (electrodul pozitiv) i L i F legai mpreun (electrodul negativ)

aVF perpendicular pe DI culege diferena de potenial dintre F (electrodul pozitiv) i R i L legai mpreun (electrodul negativ)

V1, V2, V3, V4, V5, V6 electrodul explorator (pozitiv) este plasat succesiv pe torace n diferite zone precordiale, iar electrodul de referin (negativ, electrodul central Wilson) se realizeaz prin unirea electrozilor R, L i F exploreaz planul orizontal al inimii electrodul explorator este plasat pentru:
V1, n spaiul 4 intercostal, pe marginea dreapt a sternului V2, n spaiul 4 intercostal, pe marginea stng a sternului V3, ntre V2 i V4 V4, n spaiul 5 intercostal, pe linia medioclavicular V5, n spaiul 5 intercostal, pe linia axilar anterioar V6, n spaiul 5 intercostal, pe linia medioaxilar

Pot fi aplicate i derivaii suplimentare stngi:
V7, n spaiul 5 intercostal, pe linia axilar posterioar stng V8, tot n spaiul 5 intercostal, pe linia scapular medie stng V9, pe linia paravertebral stng, la jumtatea distanei dintre V8 i coloana vertebral.
De asemenea pot fi utile pentru diagnosticul unui infarct miocardic de ventricul drept i precordialele drepte: V3R, V4R, V5R i V6R, cu localizare simetric cu cea a precordialelor stngi
Unda P
reprezint depolarizarea atrial i este:

rotunjit, simetric, pozitiv n DII, DIII i aVF i negativ n aVR cu durata: 0,08-0,12 sec amplitudinea maxim n DII (0,25 mV) definete RITMUL SINUSAL
Intervalul PR (PQ)
cuprinde depolarizarea atrial i conducerea intraatrial i atrioventricular are durata normal: 0,12-0,20 sec se scurteaz cu creterea frecvenei cardiace (FC) durata sa crete odat cu tonusul vagal
Complexul QRS
semnific depolarizarea ventricular i este format din:

unda Q, prima und negativ, reprezint depolarizarea septului interventricular unda R, prima und pozitiv, reprezint depolarizarea simultan a ventriculului drept i a regiunii apicale i centrale a ventriculului stng unda S, a doua und negativ, este dat de depolarizarea regiunii posterobazale a ventriculului stng
Complexul QRS
n cazul prezenei mai multor unde pozitive, prima dintre ele se noteaz R, iar urmtoarele unde pozitive: R, R etc. dac complexul depolarizrii ventriculare este format doar dintr-o deflexiune negativ, se numete QS durata: 0,08-0,10 sec
Complexul QRS
amplitudinea: minimum 5 mm in derivaiile standard i minimum 10 mm n precordiale. Sub aceste valori se consider microvoltaj i peste aceste valori macrovoltaj. Deflexiunile de peste 3 mm sunt notate cu litere mari (Q; R; S), iar cele sub 3 mm cu litere mici (q, r, s)
Segmentul ST
reprezint poriunea iniial, lent a repolarizrii ventriculare

ncepe la punctul J (junction), situat la limita dintre unda S i segmentul ST, trebuie s fie situat pe linia izoelectric sau la 1mm deasupra sau dedesubt de aceasta este orizontal i izoelectric
Unda T
reprezint poriunea terminal, rapid a repolarizrii ventriculare

este rotunjit, asimetric, cu panta ascendent mai lent i cea descendent mai rapid concordant ca sens cu complexul QRS amplitudinea de aproximativ 1/3 din cea a complexului QRS
Intervalul QT
definete durata total a depolarizrii i repolarizrii ventriculare

variaz invers proporional cu frecvena cardiac valorile sale se pot corecta n funcie de frecvena cardiac (QTc), conform formulei Bazett: QTc = QT/RR, unde RR este intervalul RR n ms limita superioar a intervalului QTc este de 0,45 sec
Determinarea axului electric al inimii

Axul electric
reprezint direcia procesului de activare cardiac proiectat n derivaiile membrelor rezult din sumarea n plan frontal a vectorilor electrici generai n cursul depolarizrii i repolarizrii atriilor i ventriculilor i se reprezint sub forma unui vector n sistemul de referin hexaxial
De obicei, se determin axul depolarizrii ventriculare (AQRS) care poate fi:

normal: ntre 30 i +110 grade deviat patologic la stnga: ntre 30 i 90 grade deviat patologic la dreapta: ntre +110 i +180 grade

Pentru a calcula AQRS:
se determin suma algebric a deflexiunii maxime pozitive cu deflexiunea maxim negativ, n dou din derivaiile planului frontal care sunt perpendiculare valoarea obinut se reprezint ca vector n sistemul hexaxial, innd seama de polaritate se traseaz perpendiculare din vrful vectorilor reprezentai se unete centrul sistemului hexaxial cu punctual de intersecie a celor dou perpendiculare, rezultnd AQRS

Metode rapide pentru stabilirea axului electric al inimii:
se observ n care derivaie a planului frontal, amplitudinea QRS este maxim; derivaia respectiv corespunde poziiei axului electric
Exemple: S maxim n aVF AQRS la -90 grade R maxim n aVL AQRS la -30 grade

Metode rapide pentru stabilirea axului electric al inimii:
aspectul complexului QRS din derivaiile DI sau DIII:
aspect RI RIII AQRS normal aspect RI SIII AQRS deviat patologic la stnga aspect SI RIII AQRS deviat patologic la dreapta.

LAD
Anterior Hemiblock Inferior MI WPW right pathway Emphysema Children, thin adults RVH Chronic Lung Disease WPW left pathway Pulmonary emboli Posterior Hemiblock Emphysema Hyperkalemia Lead Transposition V-Tach RAD =+120 to +180 LAD = -30 to -90 No Mans Land Axis = -90 to +- 180
RAD
No Mans Land
Normal Axis = -30 to +120
Determinarea frecvenei cardiace

Frecvena cardiac (FC) normal de repaus este de: 60-100/minut Se ine seama de urmtoarele principii:
viteza standard de derulare a hrtiei este de 25 mm/sec FC se exprim n cicluri/minut se verific dac frecvena atrial este egal cu cea ventricular
Determinarea frecvenei cardiace

FC poate fi determinat cu ajutorul ecuaiei: 1 secund................25mm 60 secunde..............x (1 minut) x = 60x25 = 1500mm/minut. FC = 1500/intervalul R-R n mm
Determinarea rapid a frecvenei cardiace Se poate face pe baza urmtoarelor principii:

hrtia ECG este marcat prin linii subiri n ptrate mici cu latura de 1mm i linii groase n ptrate mari cu latura de 5 mm la viteza de 25 mm/sec, la 1 minut (60 secunde) corespund 1500 mm
Determinarea rapid a frecvenei cardiace
se caut pe ECG o und R suprapus peste o linie groas i se numr liniile groase dup care apare urmtoarea und R pentru a aprecia FC astfel: 300, 150, 100, 75, 60, 50
Interpretacin
del ECG
Frecuencia cardiaca : se
determina dividiendo 300 por el n de cuadrados grandes entre dos QRS seguidos .
Interpretacin
del ECG
Frecuencia cardiaca en trazado irregular:. Tomar un trazado de 25 cms

(10 segundos), contar el n de intervalos entre los QRS en ese tiempo y multiplicarlo por 6
Ritmo anormal del NSA

Taquicardia: frecuencia mayor o igual a 100 latidos / minuto
Ritmo anormal del NSA

Bradicardia: frecuencia menor o igual a 60 latidos / minuto
Vector neto de despolarizacin

En las distintas derivaciones la amplitud de los potenciales medidos y graficados en el papel depende de la orientacin del electrodo positivo en relacin al vector elctrico neto .
Vector neto de despolarizacin QRS

Sistema hexaxial se usa para determinar el potencial que registrar el ECG en cada una de las derivaciones para un vector dado
Vectores netos de despolarizacin
Corazn despolarizado parcialmente. A: vector medio de despolarizacin del QRS: tiene una direccin y largo, que determina el voltaje del potencial generado. (por ejemplo 55 y 2mV)
Para determinar la magnitud del voltaje del vector A en DI se traza una lnea perpendicular al eje de DI desde la punta de A y dibujamos el vector proyectado B
B apunta al polo + de DI: voltaje en esa derivacin es + y aproximadamente la mitad de A
Vectores netos de despolarizacin: QRS

B: proyeccin de A en DI
D: proyeccin de A en DIII
C: proyeccin de A en DII
0,01 seg
0,02 seg
0,035 seg
0,05 seg
0,06 seg
Vectores netos de despolarizacin : onda P
Vectores netos de despolarizacin : onda T
Duracin: 0,08 a 0,10 s (< 0,12 s o < 2,5 mm) Altura: < de 0,25 mV (< 2,5 mm)
Onda P
Intervalo PR
Incluye tiempo de despolarizacin auricular y de conduccin auriculoventricular y del sistema His- Purkinje
Intervalo PR
Se mide desde el inicio de la onda P hasta el inicio del complejo QRS. Duracin: desde inicio de la P al inicio del QRS, va de 0,12 a 0,20 seg

Complejo QRS:
despolarizacin ventricular. Duracin:
0,06 a 0,10 segundos
QRS: presenta diversas morfologas en diferentes derivaciones

QRS:
1 onda negativa : onda Q. 1 onda positiva : onda R. onda negativa que sigue : onda S.

QRS: .
Se utilizan maysculas o minsculas en funcin del tamao de dichas ondas. Cuando hay una sola onda negativa se denomina complejo QS
QRS
deflexin intrinsecoide: tiempo desde el inicio del QRS hasta el momento en que la onda R cambia de direccin. duracin normal <0,045 seg.
se utiliza en el diagnstico de la hipertrofia ventricular izquierda, en la dilatacin ventricular izquierda y en el hemibloqueo anterior

Segmento ST:
periodo isoelctrico que sigue al QRS.

Va desde el punto J (punto de unin del segmento ST con el QRS ) hasta el inicio de la T
Segmento ST
Tiempo entre la despolarizacin total del ventrculo y su repolarizacin
Mide 0,12 segundos o menos
Segmento ST
En la mayora de las derivaciones es plano
Debe estar al mismo nivel que el segmento TP que sigue.
Segmento ST
Ascenso o depresin del ST: sugerente de isquemia miocrdica
Segmento ST
Entre V1 y V3 presenta rpido ascenso y se fusiona con onda T difcil de identificar.
Onda T: onda asimtrica, cuya 1

mitad es una curva ms gradual que
la 2. Su orientacin coincide con la del QRS.
Onda T
representa la repolarizacin y reposo ventricular (periodo refractario) Dura aproximadamente 0,20 segundos o menos y mide 0,5 mV
Onda T
Inicio onda T : periodo refractario efectivo Se altera en una serie de patologas (HVI, infarto miocardio, alteracin cido base, hiperkalemia)

Intervalo QT:
desde inicio de QRS hasta fin de onda T. De 0,2 a 0,4 segundos. Aproximadamente 40% del R-R.
Intervalo Q-T
Representa toda la actividad ventricular.
Depende da la frecuencia cardiaca: a mayor frecuencia, menor QT (repolarizacin se acorta) Se prolonga con la edad y algunos frmacos
En aVL el QRS es positivo: el eje se encuentra a - 30.
Si aVL fuera negativo, el eje estara a + 150
Desviacin izquierda por HVI
Desviacin derecha por HVD
Bloqueo rama izquierdo
BRD
Utilidad clnica
ECG anormal
Ritmos anormales por bloqueos de la conduccin
Bloqueo sinusal El ECG se salta un latido
Bloqueo sinusal
Los complejos antes y despus del paro sinusal son normales
Bloqueo sinusal
Si bloqueo permanece: NAV inicia despolarizacin Ritmo no sinusal (no hay P) Frecuencia lenta Complejos QRS-T normales
Bloqueo sinusal con ritmo del ndulo AV
2. Bloqueo auriculoventricular
NAV: nico paso entre As y Vs. Causas: 1. Isquemia del NAV o Haz de His 2. Inflamacion NAV o Haz de His (miocarditis) 3. Compresin externa del NAV o Haz de Hiz
Bloqueo AV
Bloqueo auriculoventricular
Tipos:
1. Bloqueo AV de primer grado
2. Bloqueo AV de 2 grado
3. Bloqueo AV de tercer grado
Bloqueo AV de primer grado

La conduccin por el NAV est retrasada, pero el impulso se propaga y excita los ventrculos de manera normal. Existe una onda P por cada complejo QRS.
Bloqueo AV de primer grado

Ritmo sinusal normal Onda P normal Complejo QRS normales Prolongacin del intervalo PR : mayor a 0,20 segundos.
Bloqueo AV de 2 grado
Conduccin elctrica por NAV lenta. Algunos impulsos no se conducen . Onda P sin QRS
Bloqueo AV de 2 grado tipo Mobitz I

impulsos conducidos con un intervalo PR variable, generalmente tipo Wenckebach: Los intervalos PR alargan progresivamente hasta que un impulso no se conduce.
Bloqueo AV de 2 grado tipo Mobitz I

El latido que no se conduce est entre dos ondas P. Los intervalos RR son cada vez ms cortos hasta que un impulso no se conduce
Bloqueo AV de 2 grado tipo Mobitz II

ondas P no conducidas sin que haya un alargamiento del intervalo PR. Intervalos PR constantes No se conducen 2 o ms ondas P: existe relacin ondas P / QRS (2:1, 3:1, 4:1)
Bloqueo AV de 2 grado tipo Mobitz II

Precursor frecuente del bloqueo AV completo, especialmente si se acompaa de bloqueos de rama. Se asocia a isquemia
Bloqueo AV de tercer grado

Lesin severa al NAV: ningn impulso auricular llega a los ventrculos : aurculas y ventrculos estn controlados por marcapasos independientes

Ondas P normales . PR no es medible
no existe ninguna relacin entre las ondas P y los complejos QRS: disociacin auriculoventricular completa frecuencia de ondas P generalmente mayor a la de QRS

Despolarizacin ventricular es por marcapasos ectpicos : has de Hiz: 40 a 55 /minuto. QRS normales Ventricular: 20 a 40 /minuto. QRS anchos Frecuencia QRS lenta (menor a 40/minuto) regular.
Bloqueo AV completo
Ritmo de la unin (Has de Hiz)
Ritmo ventricular (Has de Hiz)
3. Bloqueos de rama
El haz de His se bifurca en las ramas derecha
e izquierda. Ambas ramas bajan a cada lado

del tabique interventricular. Justo despus de su inicio la rama izquierda
se divide en una rama anterior y otra

posterior.
En cualquiera de estas estructuras
puede bloquearse la conduccin del

estimulo
3. Bloqueos de rama
Conduccin normal: la activacin de los ventrculos se inicia en el lado izquierdo del tabique interventricular y se propaga hacia la derecha.
Bloqueo rama derecha

Puede verse en personas sanas
Se retrasa despolarizacin VD VI despolarizacin normal: 1 mitad QRS normal .
Despolarizacin es a travs de tejido no especializado. QRS ancho por mayor tiempo de despolarizacin
Diagnstico: QRS > o = 0,12 seg. 2 onda R en V1 o V2 Ondas S anchas en DI, V5 y V6 Depresin segmento ST e inversin onda T en precordiales derechas
Bloqueo rama izquierda

Se asocia a enfermedad coronaria, a HTA o miocardiopatia dilatada. Rama izquierda irrigada por arteria descendente anterior (rama coronaria izquierda) y coronaria derecha. 2-4% pacientes con IAM lo tienen
Bloqueo rama izquierda

Normalmente despolarizacin va de izquierda a derecha. En BRI va de derecha a izquierda vector del segmento ST y de la onda T es la opuesta a la del QRS
Despolarizacin es a travs de tejido no especializado. QRS ancho por mayor tiempo de despolarizacin
Diagnstico
Complejos QRS de 0,12 seg o ms.
Prdida de la onda Q septal en DI V5 y V6 . ondas R dentadas (con una muesca en la zona intermedia del complejo QRS) en DI, aVL, V5 y V6. S profunda en precordiales derechas
BCRI
ST y onda T : deflexin opuesta al QRS infradesnivel ST y T negativa en DI, aVL y V6. Lo contrario en V1, V2 y V3
KINE 639 - Dr. Green Section 3
Terminology and Definitions of Arrhythmias

Rhythm
Reading in Conover: pages 45-52, 55-170
Rhythms from the Sinus Node
Normal Sinus Rhythm (NSR)
Sinus Tachycardia: HR > 100 b/m Causes:

Withdrawal of vagul tone & Sympathetic stimulation (exercise, fight or flight) Fever & inflammation Heart Failure or Cardiogenic Shock (both represent hypoperfusion states) Heart Attack (myocardial infarction or extension of infarction) Drugs (alcohol, nicotine, caffeine)
Sinus Bradycardia: HR < 60 b/m Causes:

Increased vagul tone, decreased sympathetic output, (endurance training) Hypothyroidism Heart Attack (common in inferior wall infarction) Vasovagul syncope (people passing out when they get their blood drawn) Depression
Rhythms from the Sinus Node
Sinus Arrhythmia: Variation in HR by more than .16 seconds Mechanism:

Most often: changes in vagul tone associated with respiratory reflexes Benign variant
Causes
Most often: youth and endurance training
Sick Sinus Syndrome: Failure of the hearts pacemaking capabilities Causes:

Idiopathic (no cause can be found) Cardiomyopathy (disease and malformation of the cardiac muscle) Implications and Associations Associated with Tachycardia / Bradycardia arrhythmias Is often followed by an ectopic escape beat or an ectopic rhythm
Recognizing and Naming Beats & Rhythms QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal
Atrial Escape Beat

normal ("sinus") beats
sinus node doesn't fire leading to a period of asystole (sick sinus syndrome)
p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an "atrial" beat
Recognizing and Naming Beats & Rhythms
Junctional Escape Beat
QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal
there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a "junctional" or a nodal beat
Ventricular Escape Beat
QRS is wide and much different ("bizarre") looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a ventricular beat
there is no p wave, indicating that the beat did not originate anywhere in the atria actually a "retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles
Ectopic Beats or Rhythms beats or rhythms that originate in places other than the SA node the ectopic focus may cause single beats or take over and pace
the heart, dictating its entire rhythm
they may or may not be dangerous depending on how they affect the cardiac output
Causes of Ectopic Beats or Rhythms hypoxic myocardium - chronic pulmonary disease, pulmonary embolus ischemic myocardium - acute MI, expanding MI, angina sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,

imbalances of calcium and magnesium
bradycardia - a slow HR predisposes one to arrhythmias enlargement of the atria or ventricles producing stretch in pacemaker cells
The Re-Entry Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery
Tissues with these type of circuits may exist: in microscopic size in the SA node, AV node, or any type of heart tissue in a macroscopic structure such as an accessory pathway in WPW
The Re-Entry Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Conduction Tissue
Repolarizing Tissue (long refractory period) Fast Conduction Path Slow Recovery
1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only
The Re-Entry Mechanism of Ectopic Beats & Rhythms
Cardiac Conduction Tissue
3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
The Re-Entry Mechanism of Ectopic Beats & Rhythms
Cardiac Conduction Tissue
4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuit
Re-entry Circuits as Ectopic Foci and Arrhythmia Generators
Atrio-Ventricular Nodal Re-entry
supraventricular tachycardia
Atrial Re-entry Ventricular Re-entry
atrial tachycardia atrial fibrillation atrial flutter
ventricular tachycardia
Atrio-Ventricular Re-entry
Wolf Parkinson White supraventricular tachycardia
Clinical Manifestations of Arrhythmias many go unnoticed and produce no symptoms
palpitations ranging from noticing or being aware of ones heart
beat to a sensation of the heart beating out of the chest

if Q is affected (HR > 300) lightheadedness and syncope, fainting drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium

very rapid arrhythmias u myocardial oxygen demand r ischemia
and angina
sudden death especially in the case of an acute MI
Premature Ventricular Contractions (PVCs, VPBs, extrasystoles):

A ventricular ectopic focus discharges causing an early beat Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre" QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion PVCs are sometimes described by lay people as skipped heart beats
R on T phenomemon
Multifocal PVC's
Compensatory pause after the occurance of a PVC
Recognizing and Naming Beats & Rhythms Characteristics of PVC's PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave) T-waves for PVCs are usually large and opposite in polarity to terminal QRS Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle Every other beat being a PVC (bigeminy) may indicate coronary artery disease Some PVCs come between 2 normal sinus beats and are called interpolated PVCs
The classic PVC note the compensatory pause
Interpolated PVC note the sinus rhythm is undisturbed
Recognizing and Naming Beats & Rhythms PVC's are Dangerous When:
They are frequent (> 30% of complexes) or are increasing in frequency The come close to or on top of a preceding T-wave (R on T) Three or more PVC's in a row (run of V-tach) Any PVC in the setting of an acute MI PVC's come from different foci ("multifocal" or "multiformed")
These dangerous phenomenon may preclude the occurrence of deadly arrhythmias: Ventricular Tachycardia The sooner defibrillation takes place, Ventricular Fibrillation
the increased likelihood of survival

R on T phenomenon
time
sinus beats
V-tach
Unconverted V-tach r V-fib
Notes on V-tach:
Causes of V-tach Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) Typical V-tach patient MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm) V-tach complexes are likely to be similar and the rhythm regular Irregular V-Tach rhythms may be due to to:
breakthrough of atrial conduction atria may capture the entire beat beat an atrial beat may merge with an ectopic ventricular beat (fusion beat)
Fusion beat - note pwave in front of PVC and the PVC is narrower than the other PVCs this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal.
Premature Atrial Contractions (PACs):

An ectopic focus in the atria discharges causing an early beat The P-wave of the PAC will not look like a normal sinus P-wave (different morphology) QRS is narrow and normal looking because ventricular depolarization is normal PACs may not activate the myocardium if it is still refractory (non-conducted PACs) PACs may be benign: caused by stress, alcohol, caffeine, and tobacco PACs may also be caused by ischemia, acute MIs, d electrolytes, atrial hypertrophy PACs may also precede PSVT
PAC
Non conducted PAC
Non conducted PAC distorting a T-wave
Premature Junctional Contractions (PJCs):

An ectopic focus in or around the AV junction discharges causing an early beat The beat has no P-wave QRS is narrow and normal looking because ventricular depolarization is normal PJCs are usually benign and require not treatment unless they initiate a more serious rhythm
PJC
Atrial Flutter:
A single ectopic macroreentrant focuses fire in the atria causing the fluttering baseline AV node cannot transmit all impulses (atrial rate: 250 350 per minute)
ventricular rhythm may be regular or irregular and range from 150 170 beats / minute
Q may d, especially at high ventricular rates A-fib and A-flutter rhythm may alternate these rhythms may also alternate with SVTs May be seen in CAD (especially following surgery), VHD, history of hypertension, LVH, CHF
Treatment: DC cardioversion if patient is unstable

drugs: (goal: rate control) Ca++ channel blockers to d AV conduction amiodarone to d AV conduction + prolong myocardial AP (u refractoriness of myocardium) The danger of thromboembolic events is also high in A-flutter
Multifocal Atrial Tachycardia (MAT):

Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles QRS complexes are almost identical to the sinus beats
Rate is usually between 100 and 200 beats per minute

The rhythm is always IRREGULAR P-waves of different morphologies (shapes) may be seen if the rhythm is slow If the rate < 100 bpm, the rhythm may be referred to as wandering pacemaker
Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF

Treatments: Ca++ channel blockers, b blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective)
Note different P-wave morphologies when the tachycardia begins
Note IRREGULAR rhythm in the tachycardia
Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT):

A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC)
QRS complexes are almost identical to the sinus beats

Rate is usually between 150 and 250 beats per minute The rhythm is always REGULAR Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q)
Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter

May be terminated by carotid massage u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockers
Rhythm usually begins with PAC
Note REGULAR rhythm in the tachycardia
ARRHYTHMIA
Edited by Yingmin Chen
Definition of Arrhythmia: The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormally.
Anatomy of the conducting system
Pathogenesis and Inducement of Arrhythmia
Some physical condition Pathological heart disease Other system disease Electrolyte disturbance and acid-base imbalance Physical and chemical factors or toxicosis
Mechanism of Arrhythmia
1. 2. 3.
1. 2.
Abnormal heart pulse formation Sinus pulse Ectopic pulse Triggered activity Abnormal heart pulse conduction Reentry Conduct block
Classification of Arrhythmia
Abnormal heart pulse formation
1. 2. 3. 4. 1. 2. 3. 4.
Sinus arrhythmia Atrial arrhythmia Atrioventricular junctional arrhythmia Ventricular arrhythmia
Abnormal heart pulse conduction

Sinus-atrial block Intra-atrial block Atrio-ventricular block Intra-ventricular block
Abnormal heart pulse formation and conduction
Diagnosis of Arrhythmia
Medical history Physical examination Laboratory test
Therapy Principal
Pathogenesis therapy Stop the arrhythmia immediately if the hemodynamic was unstable Individual therapy
Anti-arrhythmia Agents
Anti-tachycardia agents Anti-bradycardia agents
Anti-tachycardia agents
Modified Vaugham Williams classification I class: Natrium channel blocker II class: -receptor blocker III class: Potassium channel blocker IV class: Calcium channel blocker Others: Adenosine, Digital
1. 2. 3.
4.
5.
Anti-bradycardia agents
1. -adrenic receptor activator
2. M-cholinergic receptor blocker 3. Non-specific activator
Clinical usage
Anti-tachycardia agents:
Ia class: Less use in clinic 1. Guinidine 2. Procainamide 3. Disopyramide: Side effect: like Mcholinergic receptor blocker
Ib class: Perfect to ventricular tachyarrhythmia 1. Lidocaine 2. Mexiletine
Ic class: Can be used in ventricular and/or supra-ventricular tachycardia and extrasystole. 1. Moricizine 2. Propafenone
II class: -receptor blocker
1. Propranolol: Non-selective 2. Metoprolol: Selective 1-receptor
blocker, Perfect to hypertension and coronary artery disease patients associated with tachyarrhythmia.
III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent. Amioarone: Perfect to coronary artery disease and heart failure patients Sotalol: Has -blocker effect Bretylium
IV class: be used in supraventricular tachycardia 1. Verapamil 2. Diltiazem Others: Adenosine: be used in supraventricular tachycardia
Anti-bradycardia agents
Isoprenaline Epinephrine Atropine Aminophylline
Proarrhythmia effect of antiarrhythmia agents

Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patients III class: Like Ia, Ic class agents II, IV class: Bradycardia
Non-drug therapy
Cardioversion: For tachycardia especially hemodynamic unstable patient Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL) Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.
Sinus Arrhythmia
Sinus tachycardia
Sinus rate > 100 beats/min (100-180) Causes: 1. Some physical condition: exercise, anxiety, exciting, alcohol, coffee 2. Some disease: fever, hyperthyroidism, anemia, myocarditis 3. Some drugs: Atropine, Isoprenaline Neednt therapy
Sinus Bradycardia
Sinus rate < 60 beats/min Normal variant in many normal and older people Causes: Trained athletes, during sleep, drugs (-blocker) , Hypothyriodism, CAD or SSS Symptoms: 1. Most patients have no symptoms. 2. Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope. Neednt specific therapy, If the patient has severe symptoms, planted an pacemaker may
Sinus Arrest or Sinus Standstill

Sinus arrest or standstill is recognized by a pause in the sinus rhythm. Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, -blocks). Symptoms: dizziness, amaurosis, syncope Therapy is same to SSS
Sinoatrial exit block (SAB)

SAB: Sinus pulse was blocked so it couldnt active the atrium. Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al. Symptoms: dizziness, fatigue, syncope Therapy is same to SSS
Sinoatrial exit block (SAB)

Divided into three types: Type I, II, III Only type II SAB can be recognized by EKG.
Sick Sinus Syndrome (SSS)

SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction. Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease. With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms Bradycardia-tachycardia syndrome
EKG Recognition:
1. Sinus bradycardia, 40 bpm;
2. Sinus arrest > 3s

3. Type II SAB 4. Nonsinus tachyarrhythmia ( SVT, AF
or Af). 5. SNRT > 1530ms, SNRTc > 525ms 6. Instinct heart rate < 80bmp

Therapy:
1. Treat the etiology 2. Treat with drugs: anti-bradycardia
agents, the effect of drug therapy is not good. 3. Artificial cardiac pacing.
Atrial arrhythmia
Premature contractions
The term premature contractions are used to describe non sinus beats. Common arrhythmia The morbidity rate is 3-5%
Atrial premature contractions (APCs)

APCs arising from somewhere in either the left or the right atrium. Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia Symptoms: many patients have no symptom, some have palpitation, chest incomfortable. Therapy: Neednt therapy in the patients without heart disease. Can be treated with -blocker, propafenone, moricizine or verapamil.
Atrial tachycardia
Classify by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (CAT). Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; electrolytic disturbance.
Atrial tachycardia
May occur transient; intermittent; or persistent. Symptoms: palpitation; chest uncomfortable, tachycardia may induce myopathy. Auscultation: the first heart sound is variable
Intra-atrial reentry tachycardia (IART)

1. 2. 3. 4. 5.
ECG characters: Atrial rate is around 130-150bpm; P wave is different from sinus P wave; P-R interval 0.12 Often appear type I or type II, 2:1 AV block; EP study: atrial program pacing can induce and terminate tachycardia
Automatic atrial tachycardia (AAT)

1. 2. 3. 4. 5. 6.
ECG characters: Atrial rate is around 100-200bpm; Warmup phenomena P wave is different from sinus P wave; P-R interval 0.12 Often appear type I or type II, 2:1 AV block; EP study: Atrial program pacing cant induce or terminate the tachycardia
Chaotic atrial tachycardia (CAT)

Also termed Multifocal atrial tachycardia. Always occurs in COPD or CHF, Have a high in-hospital mortality ( 25-56%). Death is caused by the severity of the underlying disease. ECG characters: Atrial rate is around 100-130bpm; The morphologies P wave are more than 3 types. P-P, P-R and R-R interval are different. Will progress to af in half the cases EP study: Atrial program pacing cant induce or terminate the tachycardia
1. 2. 3. 4. 5.
Therapy
IRAT: Esophageal Pulsation Modulation, RFCA, Ic and IV class anti-tachycardia agents AAT: Digoxin, IV, II, Ia and III class antitachycardia agents; RFCA CAT: treat the underlying disease, verapamil or amiodarone. Associated with SSS: Implant pacemaker.
Atrial flutter
1.
2.
3. 4.
Etiology: It can occur in patients with normal atrial or with abnormal atrial. It is seen in rheumatic heart disease (mitral or tricuspid valve disease), CAD, hypertension, hyperthyroidism, congenital heart disease, COPD. Related to enlargement of the atria Most AF have a reentry loop in
Atrial flutter
Symptoms: depend on underlying disease, ventricular rate, the patient is at rest or is exerting With rapid ventricular rate: palpitation, dizziness, shortness of breath, weakness, faintness, syncope, may develop angina and CHF.
Atrial flutter
1. 2.
3. 4.
Therapy: Treat the underlying disease To restore sinus rhythm: Cardioversion, Esophageal Pulsation Modulation, RFCA, Drug (III, Ia, Ic class). Control the ventricular rate: digitalis. CCB, -block Anticoagulation
Atrial fibrillation
Subdivided into three types: paroxysmal, persistent, permanent. Etiology: Morbidity rate increase in older patients Etiology just like atrial flutter Idiopathic Mechanism: Multiple wavelet re-entry; Rapid firing focus in pulmonary vein, vena cava or coronary sinus.
1. 2. 3.
1. 2.
Atrial fibrillation
Manifestation: Affected by underlying diseases, ventricular rate and heart function. May develop embolism in left atrial. Have high incidence of stroke. The heart rate, S1 and rhythm is irregularly irregular If the heart rhythm is regular, should consider about (1) restore sinus rhythm; (2) AF with constant the ratio of AV conduction; (3) junctional or ventricular tachycardia; (4) slower ventricular rate may have complete AV block.
Atrial fibrillation
1. 2. 3. 4.
Therapy: Treat the underlying disease Restore sinus rhythm: Drug, Cardioversion, RFCA, Maze surgery Rate control: digitalis. CCB, -block Antithrombotic therapy: Aspirine, Warfarin
Atrioventricular Junctional arrhythmia
Atrioventricular junctional premature contractions

Etiology and manifestation is like APCs Therapy the underlying disease Neednt anti-arrhythmia therapy.
Nonparoxysmal AV junctional tachycardia

Mechanism: relate to hyperautomaticity or trigger activity of AV junctional tissue Etiology: digitalis toxicity; inferior MI; myocarditis; acute rheumatic fever and postoperation of valve disease ECG: the heart rate ranges 70-150 bpm or more, regular, normal QRS complex, may occur AV dissociation and wenckebach AV block
Nonparoxysmal AV junctional tachycardia

Therapy: Treat underlying disease; stopping digoxin, administer potassium, lidocaine, phenytoin or propranolol. Not for DC shock It can disappear spontaneously. If had good tolerance, not require therapy.
Paroxysmal tachycardia
Most PSVT (paroxysmal supraventricular tachycardia) is due to reentrant mechanism. The incidence of PSVT is higher in AVNRT (atrioventricular node reentry tachycardia) and AVRT (atioventricular reentry tachycardia), the most common is AVNRT (90%) Occur in any age individuals, usually no structure heart disease.
Manifestation:
Occur and terminal abruptly.
Palpitation, dizziness, syncope, angina, heart failure and shock. The sever degree of the symptom is related to ventricular rate, persistent duration and underlying disease
1.
2.
3.
4.
ECG characteristic of AVNRT Heart rate is 150-250 bpm, regular QRS complex is often normal, wide QRS complex is with aberrant conduction Negative P wave in II III aVF, buried into or following by the QRS complex. AVN jump phenomena
ECG characteristic of AVRT 1. Heart rate is 150-250 bpm, regular 2. In orthodromic AVRT, the QRS complex is often normal, wide QRS complex is with antidromic AVRT 3. Retrograde P wave, R-P>110ms.
1.
2. 3.
1.
2.
Therapy: AVNRT & orthodromic AVRT Increase vagal tone: carotid sinus massage, Valsalva maneuver.if no successful, Drug: verapamil, adrenosine, propafenone DC shock Antidromic AVRT: Should not use verapamil, digitalis, and stimulate the vagal nerve. Drug: propafenone, sotalol, amiodarone RFCA
Pre-excitation syndrome (W-P-W syndrome)

There are several type of accessory pathway 1. Kent: adjacent atrial and ventricular 2. James: adjacent atrial and his bundle 3. Mahaim: adjacent lower part of the AVN and ventricular Usually no structure heart disease, occur in any age individual
WPW syndrome
Manifestation: Palpitation, syncope, dizziness Arrhythmia: 80% tachycardia is AVRT, 15-30% is AFi, 5% is AF, May induce ventricular fibrillation
WPW syndrome
1.
2. 3.
4.
Therapy: Pharmacologic therapy: orthodrome AVRT or associated AF, AFi, may use Ic and III class agents. Antidromic AVRT cant use digoxin and verapamil. DC shock: WPW with SVT, AF or Afi produce agina, syncope and hypotension RFCA
Ventricular arrhythmia
Ventricular Premature Contractions (VPCs)

Etiology: 1. Occur in normal person 2. Myocarditis, CAD, valve heart disease, hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety drug) 3. electrolyte disturbance, anxiety, drinking, coffee
VPCs
Manifestation: palpitation dizziness syncope loss of the second heart sound
1. 2. 3. 4.
PVCs
Therapy: treat underlying disease, antiarrhythmia No structure heart disease: Asymptom: no therapy Symptom caused by PVCs: antianxiety agents, -blocker and mexiletine to relief the symptom. With structure heart disease (CAD, HBP): Treat the underlying diseas -blocker, amiodarone Class I especially class Ic agents should be avoided because of proarrhytmia and lack of
1. 2.
1.
2. 3.
Ventricular tachycardia
Etiology: often in organic heart disease CAD, MI, DCM, HCM, HF, long QT syndrome Brugada syndrome Sustained VT (>30s), Nonsustained VT Monomorphic VT, Polymorphic VT
Torsades de points (Tdp): A special type of polymorphic VT, Etiology: congenital (Long QT), electrolyte disturbance, antiarrhythmia drug proarrhythmia (IA or IC), antianxiety drug, brain disease, bradycardia
1.
2. 3.
4.
5. 6.
Accelerated idioventricular rhythm: 1. Related to increase automatic tone 2. Etiology: Often occur in organic heart disease, especially AMI reperfusion periods, heart operation, myocarditis, digitalis toxicity
VT
Manifestation: 1. Nonsustained VT with no symptom 2. Sustained VT : with symptom and unstable hemodynamic, patient may feel palpitation, short of breathness, presyncope, syncope, angina, hypotension and shock.
VT
ECG characteristics: 1. Monomorphic VT: 100-250 bpm, occur and terminate abruptly,regular 2. Accelerated idioventricular rhythm: a runs of 3-10 ventricular beats, rate of 60-110 bpm, tachycardia is a capable of warm up and close down, often seen AV dissociation, fusion or capture beats 3. Tdp: rotation of the QRS axis around the baseline, the rate from 160-280 bpm, QT interval prolonged > 0.5s, marked U wave
Treatment of VT
1. Treat underlying disease 2. Cardioversion: Hemodynamic
unstable VT (hypotension, shock, angina, CHF) or hemodynamic stable but drug was no effect 3. Pharmacological therapy: blockers, lidocain or amiodarone 4. RFCA, ICD or surgical therapy
Therapy of Special type VT

Accelerated idioventricular rhythm: usually no symptom, neednt therapy. Atropine increased sinus rhythm Tdp: 1. Treat underlying disease, 2. Magnesium iv, atropine or isoprenaline, -block or pacemaker for long QT patient 3. temporary pacemaker
Ventricular flutter and fibrillation

Often occur in severe organic heart disease: AMI, ischemia heart disease Proarrhythmia (especially produce long QT and Tdp), electrolyte disturbance Anaesthesia, lightning strike, electric shock, heart operation Its a fatal arrhythmia
Ventricular flutter and fibrillation

Manifestation: Unconsciousness, twitch, no blood pressure and pulse, going to die Therapy: 1. Cardio-Pulmonary Resuscitate (CPR) 2. ICD
Cardiac conduction block

Block position: Sinoatrial; intra-atrial; atrioventricular; intra-ventricular Block degree 1. Type I: prolong the conductive time 2. Type II: partial block 3. Type III: complete block
Atrioventricular Block
AV block is a delay or failure in transmission of the cardiac impulse from atrium to ventricle. Etiology: Atherosclerotic heart disease; myocarditis; rheumatic fever; cardiomyopathy; drug toxicity; electrolyte disturbance, collagen disease, levs disease.
AV Block
AV block is divided into three categories: 1. First-degree AV block 2. Second-degree AV block: further subdivided into type I and type II 3. Third-degree AV block: complete block
AV Block
Manifestations: First-degree AV block: almost no symptoms; Second degree AV block: palpitation, fatigue Third degree AV block: Dizziness, agina, heart failure, lightheadedness, and syncope may cause by slow heart rate, Adams-Stokes Syndrome may occurs in sever case.
AV Block
Treatment: 1. I or II degree AV block neednt antibradycardia agent therapy 2. II degree II type and III degree AV block need antibradycardia agent therapy 3. Implant Pace Maker
Intraventricular Block
1.
2.
3.
4.
Intraventricular conduction system: Right bundle branch Left bundle branch Left anterior fascicular Left posterior fascicular
Etiology: Myocarditis, valve disease, cardiomyopathy, CAD, hypertension, pulmonary heart disease, drug toxicity, Lenegre disease, Levs disease et al. Manifestation: Single fascicular or bifascicular block is asymptom; tri-fascicular block may have dizziness; palpitation, syncope and Adams-stokes syndrome
Therapy: 1. Treat underlying disease 2. If the patient is asymptom; no treat, 3. bifascicular block and incomplete trifascicular block may progress to complete block, may need implant pace maker if the patient with syncope
Cardiac Arrhythmias: An Update
Dr N.M.Gandhi Consultant Cardiologist Spire Gatwick Park Hospital, Horley East Surrey Hospital, Redhill Royal Sussex County Hospital, Brighton
Objectives
Identify common arrhythmias encountered by the family physician Discuss initial Mg options AF and Ventricular arrhythmias case studies Which patients needs to be referred? ECG examples
THE CONDUCTION SYSTEM
Atrial Depolarization
Ventricular Depolarization
CARDIAC ARRHYTHMIAS
Disturbances of either : Impulse generation

Impulse propagation
A R R H Y T H M I A S
ELECTROPHYSIOLOGIC PRINCIPLES
BRADYARRHYTHMIAS
SINUS NODE DYSFUNCTION AV CONDUCTION DISTURBANCES TACHYARRHYTMIAS ATRIAL TACHYCARDIAS VENTRICULAR TACHYCARDIA
Bradyarrhythmias
Impulse formation:
Decreased automaticity: Sinus bradycardia
Impulse conduction:
Conduction blocks: 1, 2, 3 AV blocks
Tachyarrythmias
Impulse formation
Enhanced automaticity:
Sinus node: sinus tachycardia Ectopic focus: Ectopic atrial tachycardia
Triggered activity
Early afterdepolarization: torsades de pointes Digitalis-induced SVT
Impulse conduction
Reentry: Paroxysmal SVT, atrial flutter and fibrilation, ventricular tachycardia and fibrillation.
Normal Sinus Rhythm
www.uptodate.com
Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.
EKG Characteristics:
Regular narrow-complex rhythm
Rate 60-100 bpm

Each QRS complex is proceeded by a P wave P wave is upright in lead II & downgoing in lead aVR
PAC
Benign, common cause of perceived irregular rhythm Can cause sxs: skipping beats, palpitations No treatment, reassurance With sxs, may advise to stop smoking, decrease caffeine and ETOH Can use beta-blockers to reduce frequency
PVC
Extremely common throughout the population, both with and without heart disease Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction
PVC
Reassurance Optimize cardiac and pulmonary disease management Beta-blocker Ablation in a small number of cases
Bradyarrhythmias
Impulse formation:
Decreased automaticity: Sinus bradycardia
Impulse conduction:
Conduction blocks: 1, 2, 3 AV blocks
Sinus Bradycardia
HR< 60 bpm; every QRS narrow, preceded by p wave Can be normal in well-conditioned athletes HR can be 30 bpm in adults during sleep, with up to 2 sec pauses
Sinus arrhythmia
Usually respiratory--Increase in heart rate during inspiration Exaggerated in children, young adults and athletesdecreases with age Usually asymptomatic, no treatment or referral Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicity Referral may be necessary if not clearly respiratory, history of heart disease
Sick Sinus Syndrome
All result in bradycardia Sinus bradycardia with a sinus pause Often result of tachy-brady syndrome: where a burst of atrial tachycardia (such as afib) is then followed by a long, symptomatic sinus pause/arrest, with no breakthrough junctional rhythm.
1st Degree AV Block
PR interval >200ms If accompanied by wide QRS, refer to cardiology, high risk of progression to 2nd and 3rd deg block Otherwise, benign if asymptomatic
2nd Degree AV Block Mobitz type I (Wenckebach)
Progressive PR longation, with eventual nonconduction of a p wave May be in 2:1 or 3:1
2nd degree block Type II (Mobitz 2)
Normal PR intervals with sudden failure of a p wave to conduct Usually below AV node and accompanied by BBB or fascicular block Often causes pre/syncope; exercise worsens sxs Generally need pacing, possibly urgently if symptomatic
3rd Degree AV Block
Complete AV disassociation, HR is a ventricular rate Will often cause dizziness, syncope, angina, heart failure Can degenerate to Vtach and Vfib Will need pacing, urgent referral
Tachyarrythmias
Impulse formation
Enhanced automaticity:
Sinus node: sinus tachycardia Ectopic focus: Ectopic atrial tachycardia
Triggered activity
Early afterdepolarization: torsades de pointes Digitalis-induced SVT
Impulse conduction
Reentry: Paroxysmal SVT, atrial flutter and fibrilation, ventricular tachycardia and fibrillation.
SUPRAVENTRICULAR T.
Sinus Tachycardia Atrial flutter Atrial fibrilation Paroxysmal Supraventricular Multifocal Atrial T. Preexcitation Syndrome (Wolff-Parkinson-white Sy.)
Sinus tachycardia
HR > 100 bpm, regular Often difficult to distinguish p and t waves
Paroxysmal Supraventricular T.
Sudden onset and termination Atrial rates of 140 to 250 /min Normal QRS complexes The mechanism is most often reentry.
Paroxysmal Supraventricular Tachycardia
Refers to supraventricular tachycardia other than afib, aflutter and MAT Usually due to reentryAVNRT or AVRT
PSVT
CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRT Can also use CCB or beta blockers to terminate, if available Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stress
Multifocal Atrial T.
Is due to enchanced automaticity within the atria, resulting in abnormal discharges from several ectopic foci Most often occurs in the setting of severe pulmonary disease and hypoxemia. EKG: irregular rhythm with multiple (at leats 3) P waves morphologies
Atrial flutter
Is caracterized by rapid coarse sawtooth appearing atrial activity, at rate of 250 to 350 x min. Many of these fast impulses reach the AV node during its refractory period, so that the ventricular rate is generally lower. Frequently it degenerates into atrial fibrilation The most expiditious therapy is electrical cardioversion, which is undertaken directly for highly symptomatic patients. (to revert chronic refractory atrial flutter that has not responded to other approaches)
Preexcitation Syndrome
Wolff-Parkinson-White Syndrome EKG: Although different types of bypass tracts have been identified, the bundle of Kent, is the most common and can usually conduct in both the anterograde and retrograde directions.
Atrial Fibrillation
Irregular rhythm Absence of definite p waves Narrow QRS Can be accompanied by rapid ventricular response
Atrial fibrillation--management
Rhythm vs Rate controlif onset is within last 24-48 hours, may be able to arrange cardioversionuse heparin around procedure Need TEE if valvular disease (high risk of thrombus) If unable to definitely conclude onset in last 2448 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 weeks after
Atrial Fibrillation: Clinical Problems

Embolism and stroke (presumably due to LA clot) Acute hospitalization with onset of symptoms Anticoagulation, especially in older patients (> 75 yr.) Congestive heart failure
Loss of AV synchrony
Loss of atrial kick Rate-related cardiomyopathy due to rapid ventricular response
Rate-related atrial myopathy and dilatation Chronic symptoms and reduced sense of well-being
AF: Medical Management

Treatment of underlying cause
Ventricular rate control

Anticoagulation Antiarrhythmics with a view to restore sinus rhythm
Control of Ventricular Rate in Atrial Fibrillation

Betablockers Calcium channel blockers
Verapamil, diltiazem
Digoxin
Amiodarone
Anticoagulation
Anticoagulation
Assessment of bleeding risk should be part of the clinical assessment of AF patients prior to starting anticoagulation
Antithrombotic benefits and potential bleeding risks of long-term coagulation should be explained and discussed with the patient
Aim for a target INR of between 2.0 and 3.0
NICE 2006
CHADS 2 scoring
CCF Hypertension Age > 75 Diabetes Stroke/TIA 1 point 1 point 1point 1 point 2 points
Any patients with AF with a score of =/>2 would benefit from being on Warfarin
Cardioversion
Cardioversion
Cardioversion results in SR in at least 90% of cases
SR is only maintained in 30-50% at one year Class 1a, 1c and III agents increase likelihood of maintained SR from 30-50% to 50-70% at one year
Follow-up
Follow-up after cardioversion should take place at 1 month, and the frequency of subsequent reviews should be tailored to the patient Reassess the need for anticoagulation at each review
Catheter Ablation for AF
AF Ablation
Success rates approx 70% but may require repeat procedure Often increase in symptoms for first 3-6 months after procedure does not indicate failure
Risks damage to existing conduction mandating pacing Cardiac perforation/tamponade Bleeding Stroke/thromboembolism Death
Catheter Ablation: Indications

Symptomatic patients
Refractory to Antiarrhythmics Medical therapy contraindicated due to comorbidities or intolerance
NICE 2006
Which AF patients need Specialist Referral?

Patients with: - WPW syndrome - Uncontrolled ventricular rate (> 200/min) - Tachy-brady syndrome - For rhythm control strategy - CCF - Intolerant to Drugs - Invasive options
VENTRICULAR ARRHYTHMIAS
Ventricular tachycardia Torsades De Pointes
Ventricular fibrillation
Is divided in 2 categories:
If it persist for more than 30 seconds sustained VT Less than 30 seconds: nonsustained VT
Symptoms vary depending on the duration.

Major manifestations are hypotension and loss of consciousness.
Non-sustained ventricular tachycardia

Need to exclude heart disease with Echo and stress testing May need anti-arrhythmia treatment if sxs In presence of heart disease, increased risk of sudden death Need referral for EPS and/or prolonged Holter monitoring ICD may be life saving
Torsades De Pointes
Varying amplitudes of the QRS. It can be produced by afterdepolarizations (triggered activity). Particularly in prolonged QT interval. Occur with some drugs (quinidine), electrolite disturbances, and congenital prolongation of the QT interval.
Specialist Referral
ECG Examples
Contact...
* E-mail: nandkumar.gandhi@sash.nhs.uk drnmgandhi@hotmail.com * Fax: 01737 231938 * Phone: Spire - 01293 785511 ESH - 01737 768511, ext.6333
V mulumesc !
2. Unstable thrombotic mass (transoesophageal echocardiography) A transoesophageal view clearly shows a large thrombus (red arrow) in the left auricle that may break away at any moment.
3. Thrombus formation in the left auricle (computer graphics superimposed on in-body photograph) The irregular beating of the heart in atrial fibrillation creates ideal conditions for thrombus formation in the left auricle, especially in patients with mitral valve insufficiency.
5. Fragmentation of the thrombus (computer graphics superimposed on in-body photograph) As the size of the thrombotic mass increases, it becomes more of a threat. Especially if the heart rate is normalised, fragments of the thrombus may break away to be swept into the circulation.
6. Thrombotic material in the aortic arch (computer graphics superimposed on in-body photograph) Once fragments of the thrombus are in the blood stream they may be carried to any part of the body. Small fragments may result in a transient cerebral ischaemic attack. Larger pieces may have more devastating consequences.
7. Cerebral thromboembolism (computer graphics superimposed on in-body photograph) 25 percent of the blood flow from the heart is pumped to the brain. Cerebral thromboemboli most frequently affect the middle cerebral artery.
Atrial fibrillation ECG
1 sec
Rhythm control approaches

Electrical cardioversion Pharmacological agents Non-pharmacological approaches
Electrical cardioversion
Metal paddle ECG
Heart rhythm Cardioversion in atrial fibrillation shock
Normal heart rhythm
Recommendations for successful cardioversion:
Antiarrhythmic drugs to maintain normal sinus rhythm Anticoagulation >3 weeks before and >1 month after chemical or electrical cardioversion, or permanently if necessary Transoesophageal echocardiogram (TEE) to detect any clot in the left atrial appendage before cardioversion Successful cardioversion is more likely if the patient: - has no other cardiovascular problems - has normal sized atria - has been in atrial fibrillation for a relatively short period - had factors contributing to atrial fibrillation (e.g., hyper- or hypothyroidism)
Electrical cardioversion
Specialised equipment and expertise required Unpleasant experience for patients Good cardioversion rates but risk of immediate or long-term recurrence Pharmacological therapy required to prevent recurrences of AF
Fuster V et al. Eur Heart J 2006;27:19792030 www.medicinenet.com
Heart disease?
Maintenance therapy
Yes CAD Sotalol Amiodarone Dofetilide Disopyramide Procainamide Quinidine Hypertension
No (or minimal)
Flecainide Propafenone Sotalol
HF
Amiodarone Dofetilide
LVH greater than or equal to 1.4 cm

Yes No
Amiodarone Dofetilide
Disopyramide Procainamide Quinidine
Consider non-pharmacological options
Amiodarone
Flecainide Propafenone Amiodarone Dofetilide Sotalol
Disopyramide Procainamide Quinidine
Fuster V et al. Eur Heart J 2006;27:19792030
Ablation and surgical procedures

Elective percutaneous
Catheter ablation
Paroxysmal AF Various technologies Promising technique under development
Intraoperative ablation
Open-heart surgery for another indication Concomitant treatment Ablation radiofrequency, laser, cryotherapy Long-term efficacy 6070%
Maze procedure
Persistent/permanent AF Open-heart surgery Primary treatment of AF Selected, highly symptomatic patients Long-term curative efficacy >90%
Permanent pacemaker therapy

AF is not an accepted indication unless bradycardia is present Moderately effective in some patients Highly effective in some patients with strictly vagal AF Specific preventive algorithms under development
Ventricular rate control

Pharmacological agents Surgical procedures with
device implantation
Rate control - calcium channel blockers

Verapamil, diltiazem Reduce contractions by blocking the entry of calcium into heart cells
Preferred in patients with heart or lung disease Verapamil most commonly prescribed
Can cause prolonged hypotension
Rate control - -blockers:

E.g. propranolol, atenolol
Decrease sensitivity to adrenaline
Preferred for young, active patients

Not suitable for patients with asthma Can cause hypotension and bradycardia
Rate control - digoxin

Most widely prescribed for rate control Promotes AF by shortening atrial refractory period Slow onset of effect Little effect on ventricular rate in active patients Sometimes used for conversion or prevention of recurrence of AF lack of
Ventricular rate control ablation and device implantation

Transvenous His ablation Persistent/permanent AF Patients with insufficient rate control Permanent pacemaker needed
Anticoagulation therapy needed
Implant devices pacemaker
Atrial fibrillation episodes are triggered by atrial premature beats (APBs) with short coupling intervals APBs from pulmonary veins may perpetuate atrial fibrillation
Implant devices pacemaker Batterypowered generator Pacer wire
Pacemaker
Battery-powered generator and pacer wires Pacing algorithms detect APBs and begin pacing after
a premature beat
Implant devices implantable defibrillators Cardioverter Implanted

Defibrillator
Electrode charge
Defibrillators for ventricular as well as atrial fibrillation now

available
Different pacing modalities combined with defibrillation Can be activated manually by patient or physician when
sedation is adequate
Percutaneous treatments transvenous His ablation

Catheter with electrode Pulmonary Veins Left Atrium Right Atrium
Catheter with electrode is guided to the pulmonary vein ostia in the left atrium
Electrode burns off (or isolates) pulmonary vein

Percutaneous invasive catheter ablation aiming at destruction of the AV node, which will result in an AV block III and permanent pacemaker dependence. The patient will be free from symptoms of atrial fibrillation, that will continue in the atria. Anticoagulation is still needed. Transvenous His ablation is an option in selected elderly patients with persistent/ permanent atrial fibrillation with ineffective rate control
Percutaneous treatments percutaneous elective catheter ablation

Catheter with electrode
Target is pulmonary vein
Pulmonary Veins Left Atrium
Right Atrium
Catheter with electrode is guided to the pulmonary vein ostia in the left atrium
Electrode burns off (or isolates) pulmonary vein

Percutaneous elective catheter ablation (pulmonary vein isolation) is available as an experimental treatment and exists in two main varieties. The aim is cure or a very substantial reduction of the time in atrial fibrillation. At present about 60% of the patients experience cure and another 20% improved symptoms. The procedure is only available at specialised arrhythmia clinics and is used for selected, very symptomatic patients
Surgical techniques isolation of pulmonary veins

Both ablation and surgery of the pulmonary
veins are newly introduced, specialised techniques
Currently appropriate for selected patients

only
Surgical techniques maze procedure

Incisions
Incisions made in atrium to block small

re-entrant circuits
Barrier from incisions allow only one major

electrical route from top to bottom of the heart
Cardiac Arrhythmias II: Tachyarrhythmias

Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director, Electrocardiography Laboratory
Supraventricular Tachycardias
(Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region)
QRS typically narrow (in absence of bundle branch block); thus, also termed narrow QRS tachycardia
Supraventricular Tachycardia (SVT) Terminology
Usually paroxysmal, i.e, starting and stopping abruptly; in which case, called PSVT Paroxysmal Atrial Tachycardia (PAT) the older term for PSVT - is misleading and should be abandoned
AV Junctional Reentrant Tachycard (typically incorporate AV nodal tissu
Mechanism of Reentry
Bidirectional Conduction
Unidirectional Block
Recovery of Excitability & Reentry
AV Nodal Reentrant Tachycardia
AV Nodal Reentrant Tachycardia Circuit

F = fast AV nodal pathway S = slow AV nodal pathway
(His Bundle)
During sinus rhythm, impulse conduct preferentially via the fast pathway
Initiation of AV Nodal Reentrant Tachycardia

PAC
PAC
PAC = premature atrial complex (beat)
Sustainment of AV Nodal Reentrant Tachycardia

Rate 150-250 beats per min
P waves generated retrogradely (AV node atria) and fall within or at tail of QRS
Sustained AV Nodal Reentrant Tachycardia

V1
Note fixed, short RP interval mimicking r deflection of QRS
Orthodromic AV Reentrant Tachycardia
AP
Retrograde conduction via accessory pathway (AP)
Anterogade conduction via normal pathway
Initiation of Orthodromic AV ReentrantTachycardia

PAC
Atria
AP AVN
Ventricles
PAC = premature atrial complex (beat)
Sustainment of Orthodromic AV Reciprocating Atria Tachycardia

AP AVN
Rate 150-250 beats per min
Ventricles
Retrograde Ps fall in the ST segment with fixed, short RP
Sinus beat
Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome)

Delta Wave Hybrid QRS shape
AP
PR < .12 s
Fusion activation of the ventricles
QRS .12 s
Varying Degrees of Ventricular Preexcitation
QRS Width: Synchronous vs. Asynchronous Ventricular Activation

QRS Normal synchronous overlapping activation of both ventricles: On time Late Wide On time (or late) Narrow
Asynchronous scenario I:
Head start Asynchronous scenario II:
Wide
Intermittent Accessory Pathway Conduction

V Preex Normal Conduction V Preex
Note all-or-none nature of AP conduction
Orthodromic AV Reentrant Tachycardia

NSR with V Preex
SVT: V Preex gone
Note retrograde P waves in the ST segment
Concealed Accessory Pathway

Sinus beat
No Delta wave during NSR (but AP capable of retrograde conduction)
Summary of AV Junctional Reentrant Tachycardias

Reentrant circuit incorporates AV nodal tissue
P waves generated retrogradely over a fast pathway

Short, fixed RP interval
Clinical Significance of AV Junctional Reentrant Tachycardias Rarely life-threatening

However, may produce serious symptoms (dizziness or syncope [fainting]) Can be very disruptive to quality of life Involvement of an accessory pathway can carry extra risks
Atrial Tachyarrhythmias
Sinus Tachycardia (100 to 180+ beats/min)
P waves oriented normally PR usually shorter than at rest
Causes of Sinus Tachycardia

Hypovolemia ( blood loss, dehydration) Fever Respiratory distress Heart failure Hyperthyroidism Certain drugs (e.g., bronchodilators) Physiologic states (exercise, excitement, etc)
Premature Atrial Complex (PAC)

V5 Non-Compensatory Pause
Timing of Expected P
Premature Atrial Complex (PAC): Alternative Terminology

Premature atrial contraction Atrial extrasystole
Atrial premature beat

Atrial ectopic beat
Atrial premature depolarization
PACs: Bigeminal Pattern

P
Note deformation of T wave by the PAC

Regularly Irregular Rhythm
PACs with Conduction Delay/Block

P P
Physiologic AV Block
Physiologic AV Delay
Recovered AV Conduction
PAC with Aberrant Conduction (Physiologic Delay in the His Purkinje V1 System)
P P P P
RBBB
PACs with Aberrant Conduction (Physiologic RBBB and LBBB)

V1
RBBB
LBBB
Normal conduction
PACs with Physiologic LBBB and His-Purkinje System Block
V1 Non-conducted PAC
Non-Conducted PAC
V5
V1 P P P P
Note deformation of T wave by the PAC
Bigeminal/Blocked PACs Mimicking Sinus Bradycardia

V1
Only the 4th bigeminal PAC conducts
Clinical Significance PACs

Common in the general population May be associated with heart disease Can be a precursor to atrial tachyarrhythmias
Atrial Tachycardia
V1
Differs from AV nodal or AV reentrant SVT
RP intervals can be variable RP often > PR (Example slower than more common rate beats per min)
Clinical Significance of Atrial Tachycardia

Similar to sequela of AV junctional reentrant tachycardias
Must be differentiated from them diagnostically
Atrial Flutter (Typical, Counterclockwise)

Reentrant mechanism
Atrial Flutter
II Classic inverted sawtooth flutter waves at 300 min-1 (best seen in II, III and AVF)
4:1
V1
2:1
Note variable ventricular response
Atrial Flutter
2:1 Conduction (common) V. rate 140-160 beats/min
2:1 & 3:2 Conduction
1:1 Conduction (rare but dangerous)
Atrial Fibrillation
Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min
Atrial Fibrillation
V5
V1
Rapid, undulating baseline (best seen in V1) Most impulses block in AV node Erratic conduction
Atrial Fibrillation: Characteristic Irregularly Irregular Ventricular Response

II
Atrial Fibrillation with Rapid Ventricular Response

II
Irregularity may be subtle
Atrial Fibrillation: Autonomic Modulation Baseline of Ventricular Response
Immediately after exercise
Clinical Significance of Atrial Flutter and Fibrillation

Causes
Usually occur in setting of heart disease; but sometimes see lone atrial fibrillation Hyperthyroidism (atrial fibrillation)
May acutely precipitate myocardial ischemia or heart failure Chronic uncontolled rates may induce cardiomyopathy and heart failure Both can predispose to thromboembolic stroke, etc
Varying Degrees of Ventricular Preexcitation
Atrial Fibrillation with Rapid Conduction Via Accessory Pathway
V1
Atrial Fibrillation with Third Degree AV Block
V5
Regular ventricular rate reflects dissociated slow junctional escape rhythm
Regular Narrow QRS Tachycardias
Differential Diagnosis of Regular Narrow QRS (Supraventricular) Tachycardia

Reentrant SVT incorporating AV nodal tissue
AV nodal reentrant tachycardia Orthodromic AV reentrant tachycardia
SVT mechanism confined to the atria

Sinus tachycardia Atrial flutter Other regular atrial tachycardias
Short-RP favors AV node-dependent
Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal Conduction

Vagotonic Maneuvers
Carotid sinus massage Valsalva maneuver (bearing down) Facial ice pack (diving reflex; for kids)
Adenosine (6-12 mg I.V.) If SVT breaks, a reentrant mechanism involving the AV node is likely If atrial rate unchanged, but ventricular rate slows (#Ps > #QRSs), SVT is atrial in origin
SVT Responses to AV Nodal Depressant Maneuvers

SVT termination
AV nodal reentrant tachycardia Orthodromic AV reentrant tachycardia
No SVT termination (despite maximal attempts)

Sinus tachycardia Atrial flutter or fibrillation Most atrial tachycardias (a minority are adenosine-sensitive)
Carotid Sinus Massage

Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes
Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage)
SVT
Carotid Sinus Massage
SVT
Adenosine 6 mg
P P P P
Ventricular Tachyarrhythmias
Premature Ventricular Complex (PVC): Alternative Terminology

Premature ventricular contraction Ventricular extrasystole
Ventricular premature beat

Ventricular ectopic beat
Ventricular premature depolarization
Premature Ventricular Complex (PVC)
Compensatory Pause
QRS Width: Synchronous vs. Asynchronous Ventricular Activation

QRS Normal synchronous overlapping activation of both ventricles: On time Late Wide On time (or late) Narrow
Asynchronous scenario I:
Head start Asynchronous scenario II:
Wide
PVCs: Bigeminal Pattern
Regularly Irregular Rhythm
Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but 100 bpm)
Fusion beat Ectopic ventricular activation
Sinus acceleration
Normal ventricular activation
AV Dissociation
ATRIA AND VENTRICLES ACT INDEPENDENTLY SA Node
Ventricular Focus
Ventricular Tachycardia (VT)

V1
Rates range from 100-250 beats/min Non-sustained or sustained P waves often dissociated (as seen here)
Ladder Diagram of AV Dissociation During Ventricular Tachycardia

Slower atrial rate
Faster ventricular rate Impulses invade the AV node retrogradely and anterogradely, creating physiologic interference and block. Under the right conditions, some anterograde impulses may slip through.
This phenomenon is not equivalent to third degree AV block
Ladder Diagram of AV Dissociation During Third Degree AV Block Faster atrial rate
Slower ventricular (escape) rhythm
Note that impulses block anterogradely and retrogradely within the AV conduction system
Monomorphic VT
Polymorphic VT
V1
Causes of PVCs and VT

PVCs are fairly common in normals but are also seen in the setting of heart disease Monomorphic VT often implies heart disease, but can sometimes be seen in structurally normal hearts Polymorphic VT can result from myoardial ischemia or conditions that prolong ventricular repolarization Electrolyte derangements, hypoxemia and
MI Scar-Related Sustained Monomorphic VT Circuit
Torsade de Pointes (Polymorphic VT Associated with Prolonged Repolarization)
Clinical Significance of PVCs and VT

Can be a tip-off to underlying cardiac, respiratory or metabolic disorder VT may (but need not invariably) lead to hemodynamic collapse or more lifethreatening ventricular tachyarrhythmias, increasing the risk of cardiac arrest
Ventricular Flutter
VT 250 beats/min, without clear isoelectric line Note sine wave-like appearance
Ventricular Fibrillation (VF)
Totally chaotic rapid ventricular rhythm Often precipitated by VT Fatal unless promptly terminated (DC shock)
Sustained VT: Degeneration to VF
Atrial Fibrillation with Rapid Conduction Via Accessory Pathway: Degeneration to VF
Diagnosing Regular Wide QRS Tachycardia
Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction?

V1
Sustained Aberrant Conduction

V1
Clinical Clues to Basis for Regular Wide QRS Tachycardia

REMEMBER: VT does not invariably cause hemodynamic collapse; patients may be conscious and stable History of heart disease, especially prior myocardial infarction, suggests VT Occurrence in a young patient with no known heart disease suggests SVT 12-lead EKG (if patient stable) should be obtained
Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction?
More R-Waves Than P-Waves Implies VT!

II
Artifact Mimicking Ventricular Tachycardia

QRS complexes march through the pseudo-tachyarrhythmia
Artifact precedes VT
Limitations of rate control

Atrial fibrillation still present normal sinus rhythm not restored Careful dose titration required
Administration with 2 or more ratecontrol agents is common Can cause sick sinus syndrome in patients with a diseased AV node

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ELECTROCARDIOGRAMA NORMAL

Conducerea impulsului electric n inim

Conducerea impulsului electric n inim

Conducerea impulsului electric n inim

Conducerea impulsului electric n inim

Classification of Electrocardiogram (ECG) Waveforms for the Detection of Cardiac Problems

Pozitionare electrozi periferici

Derivaiile unipolare ale membrelor

Derivaiile standard ale membrelor

Derivaiile standard ale membrelor

Derivaiile standard ale membrelor

Derivaiile unipolare ale membrelor

Derivaiile unipolare ale membrelor

Derivaiile unipolare ale membrelor

Triunghiul lui Einthoven

Derivaiile unipolare precordiale

Se debe medir la duracin y voltaje de los complejos y ondas

Se debe medir la duracin y voltaje de los complejos y ondas

Valores normales de voltaje y duracin

Valores normales de voltaje y duracin

0,06 a 0,10 segundos

QRS: presenta diversas morfologas en diferentes derivaciones

Valores normales de voltaje y duracin

Valores normales de voltaje y duracin

Valores normales de voltaje y duracin

periodo isoelctrico que sigue al QRS.

Debe estar al mismo nivel que el segmento TP que sigue.

Ascenso o depresin del ST: sugerente de isquemia miocrdica

Valores normales de voltaje y duracin

Onda T: onda asimtrica, cuya 1

Valores normales de voltaje y duracin

80-100 mseg 350-440 mseg

Health and Safety

Derivaiile standard ale membrelor

Derivaiile unipolare ale membrelor

Derivaiile unipolare ale membrelor

Derivaiile unipolare precordiale

Derivaiile unipolare precordiale

reprezint depolarizarea atrial i este:

semnific depolarizarea ventricular i este format din:

reprezint poriunea iniial, lent a repolarizrii ventriculare

reprezint poriunea terminal, rapid a repolarizrii ventriculare

definete durata total a depolarizrii i repolarizrii ventriculare

Determinarea axului electric al inimii

De obicei, se determin axul depolarizrii ventriculare (AQRS) care poate fi:

Determinarea axului electric al inimii

Determinarea axului electric al inimii

Determinarea axului electric al inimii

Determinarea axului electric al inimii

Normal Axis = -30 to +120

Determinarea frecvenei cardiace

Determinarea frecvenei cardiace

Determinarea rapid a frecvenei cardiace Se poate face pe baza urmtoarelor principii:

Determinarea rapid a frecvenei cardiace

Frecuencia cardiaca en trazado irregular:. Tomar un trazado de 25 cms

Ritmo anormal del NSA

Ritmo anormal del NSA

Vector neto de despolarizacin

Vector neto de despolarizacin QRS

Vectores netos de despolarizacin

Vectores netos de despolarizacin

Vectores netos de despolarizacin

B apunta al polo + de DI: voltaje en esa derivacin es + y aproximadamente la mitad de A

Vectores netos de despolarizacin: QRS