curs ecg
DESCRIPTION
Curs ECGTRANSCRIPT
ELECTROCARDIOGRAMA ELECTROCARDIOGRAMA NORMALNORMALĂĂ
ELECTROCARDIOGRAMAELECTROCARDIOGRAMA
1) Definiţie
2) Istoric
3) Principiu
4) Electrozi şi derivaţii
5) Analiza ECG
ELECTROCARDIOGRAMAELECTROCARDIOGRAMA
1) Definiţie
2) Istoric
3) Principiu
4) Electrozi şi derivaţii
5) Analiza ECG
DEFINIŢIEDEFINIŢIE
Rezultatul modificărilor electrice care Rezultatul modificărilor electrice care activează contracţia atriilor şi activează contracţia atriilor şi ventriculilorventriculilor
Reprezintă înregistrarea la suprafaţa Reprezintă înregistrarea la suprafaţa corpului a variaţiilor de potenţial ale corpului a variaţiilor de potenţial ale câmpului electric cardiaccâmpului electric cardiac,, produse de produse de depolarizarea şi repolarizarea celulelor depolarizarea şi repolarizarea celulelor miocardicemiocardice
ELECTROCARDIOGRAMAELECTROCARDIOGRAMA
1. Definiţie
2. Istoric
3. Principiu
4. Electrozi şi derivaţii
5. Convenţii în electrocardiografie
6. Electrogeneza undelor ECG
7. Analiza ECG
ISTORICISTORIC
1791 Galvani a emis teoria ”electricităţiianimale”
1792 Volta – electricitatea se datorează conţinutului organismelor în metale şi diferenţa de concentraţie a acestora generează curentul electric
Entuziasm – folosirea curentului electric pentru reanimarea unor decedaţi (studii pe criminali spânzuraţi)
ISTORICISTORIC
1887 Fiziologul britanic Augustus D. Waller din Londra a publicat primele studii de electrocardiografie umană, realizate cu un electrometru capilar
1889 Fiziologul olandez Willem Einthoven l-a văzut pe Waller demonstrându-şi experimentul cu ocazia Primului Congres al Fiziologilor din Bale. – Jimmy
1890 GJ Burch din Oxford a imaginat un dispozitiv de corectare a oscilaţiilor electrometrului
1893 Willem Einthoven introduce termenul de “electrocardiogramă” la întrunirea Asociaţiei Medicale Olandeze
ISTORICISTORIC
1901– Einthoven inventează un nou dispozitiv pentru
înregistrarea EKG, din electrozi din argint
1924– Willem Einthoven câştigă premiul Nobel pentru
inventarea electrocardiografului
HeartHeart
Conducerea impulsului electric în Conducerea impulsului electric în inimăinimă
Este realizată de către Este realizată de către ţesutul nodal al inimii ţesutul nodal al inimii format din:format din:
– Nodul sino-atrialNodul sino-atrial
– Nodul atrio-ventricularNodul atrio-ventricular
– Fasciculul HissFasciculul Hiss
– Reţeaua PurkinjeReţeaua Purkinje
Conducerea impulsului electric în inimăConducerea impulsului electric în inimă
Nodul sino-atrialNodul sino-atrial este format dintr-un este format dintr-un grup de celule grup de celule specializate, cu specializate, cu proprietatea de a proprietatea de a descărca descărca automat automat impulsuri electriceimpulsuri electrice ((principalulprincipalul pacemakerpacemaker al inimiial inimii) ) aflat la nivelul aflat la nivelul atriului dreptatriului drept
Conducerea impulsului electric în inimăConducerea impulsului electric în inimă
Mai multe Mai multe căi căi internodaleinternodale fac fac legătura între NSA şi legătura între NSA şi nodul atrio-nodul atrio-ventricularventricular (NAV) (NAV)
Conducerea impulsului electric în inimăConducerea impulsului electric în inimă
Aceste fibre se Aceste fibre se continuă apoi spre continuă apoi spre apex unde se împart apex unde se împart în mai multe în mai multe fibre fibre PurkinjePurkinje mici care mici care se distribuie se distribuie celulelor contractile celulelor contractile ventriculareventriculare
PRINCIPIUPRINCIPIU
Inima poate fi considerată o baterie, un generator de curent electric inclus într-un volum conductor (corp)
Inima generează un câmp electric ce poate fi evidenţiat la suprafaţa corpului, prin electrozi plasaţi pe tegument
PRINCIPIUPRINCIPIU
Depolarizare şi Repolarizare
În repaus, cardiomiocitele sunt încărcate pozitiv pe versantul extern al membranei şi negativ la interior
În timpul depolarizării, potenţialul de membrană se inversează. Negativitatea de repaus a interiorului se reduce spre 0 şi apoi interiorul devine pozitiv ca urmare a influxului de Na+.
Potenţialul de acţiunePotenţialul de acţiune
Classification of Electrocardiogram Classification of Electrocardiogram (ECG) Waveforms for the Detection of (ECG) Waveforms for the Detection of
Cardiac ProblemsCardiac Problems
NORMAL ECGNORMAL ECG
right left
Pozitionare electrozi periferici
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVL aVL – perpendiculară pe DIIperpendiculară pe DII– culege diferenţa de culege diferenţa de
potenţial dintre potenţial dintre LL (electrodul (electrodul pozitivpozitiv) şi ) şi RR şi şi FF legaţi legaţi împreună (electrodul împreună (electrodul negativnegativ))
Derivaţiile standard ale membrelorDerivaţiile standard ale membrelor
DI – electrodul + e plasat
pe membrul superior stâng
– electrodul – e plasat pe membrul superior drept
Derivaţiile standard ale membrelorDerivaţiile standard ale membrelor
DII – electrodul – e plasat
pe membrul superior drept
– electrodul + e plasat pe membrul inferior stâng
Derivaţiile standard ale membrelorDerivaţiile standard ale membrelor
DIII
electrodul – e plasat pe membrul superior stâng
electrodul + e plasat pe membrul inferior stâng
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVR, aVL şi aVFaVR, aVL şi aVFexplorează explorează planul frontalplanul frontal al inimii al inimiielectrodul electrodul exploratorexplorator ( (pozitivpozitiv) se plasează pe R, L sau F, iar ) se plasează pe R, L sau F, iar ceilalţi doi electroziceilalţi doi electrozi se leagă împreună, reprezentând electrodul se leagă împreună, reprezentând electrodul de referinţă (de referinţă (negativnegativ))
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVR aVR – perpendiculară pe perpendiculară pe
DIII DIII – culege diferenţa de culege diferenţa de
potenţial dintre potenţial dintre RR (electrodul (electrodul pozitivpozitiv) şi ) şi LL şi şi FF legaţi legaţi împreună (electrodul împreună (electrodul negativnegativ))
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVFaVF – perpendiculară pe DIperpendiculară pe DI– culege diferenţa de culege diferenţa de
potenţial dintre potenţial dintre FF (electrodul (electrodul pozitivpozitiv) şi ) şi RR şi şi LL legaţi legaţi împreună (electrodul împreună (electrodul negativnegativ))
Triunghiul lui Triunghiul lui EinthovenEinthoven
Derivaţiile unipolare precordialeDerivaţiile unipolare precordiale
TRIANGULO DE TRIANGULO DE EINTHOVENEINTHOVEN
Standardizarea ECGStandardizarea ECG
implică:implică:– pe pe verticalăverticală: :
1mm = 0,1mV1mm = 0,1mV, , permiţând aprecierea permiţând aprecierea amplitudiniiamplitudinii undelor undelor
– pe pe orizontalăorizontală: : 1mm = 0,04 secunde1mm = 0,04 secunde (la viteza de 25 (la viteza de 25 mm/sec), permiţând mm/sec), permiţând aprecierea aprecierea durateiduratei undelor şi intervalelorundelor şi intervalelor
ONDA PONDA P ONDA RONDA R ONDA TONDA T
ONDA QONDA Q ONDA SONDA S
Se debe medir la duración y Se debe medir la duración y voltaje de los complejos y ondasvoltaje de los complejos y ondas
Se debe medir la duración y Se debe medir la duración y voltaje de los complejos y ondasvoltaje de los complejos y ondas
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
DuraciónDuración: 0,08 a 0,10 s: 0,08 a 0,10 s (< (< 0,12 s o < 2,5 mm)0,12 s o < 2,5 mm)
Altura:Altura: < de 0,25 mV (< 2,5 < de 0,25 mV (< 2,5 mm)mm)
Onda POnda P
ECG waveformECG waveform
The QRS complex The QRS complex corresponds to corresponds to depolarization of depolarization of ventriclesventricles
Need Matlab and Need Matlab and Fourier Analysis to Fourier Analysis to develop algorithm for develop algorithm for QRSQRS
Incluye tiempo de despolarización Incluye tiempo de despolarización auricular y de conducción auricular y de conducción auriculoventricular y del sistema auriculoventricular y del sistema His- PurkinjeHis- Purkinje
Intervalo PRIntervalo PR
Intervalo PR Intervalo PR
Se mide desde el Se mide desde el inicio de la onda P inicio de la onda P hasta el inicio del hasta el inicio del complejo QRS. complejo QRS.
Duración: desde Duración: desde inicio de la P al inicio de la P al inicio del QRS, va inicio del QRS, va de 0,12 a 0,20 de 0,12 a 0,20 segseg
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Complejo Complejo QRSQRS::
despolarización despolarización ventricular.ventricular.
Duración:Duración:
0,06 a 0,10 0,06 a 0,10 segundossegundos
QRS: presenta diversas morfologías en QRS: presenta diversas morfologías en diferentes derivacionesdiferentes derivaciones
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
QRS:QRS: 1ª onda negativa : onda Q.1ª onda negativa : onda Q.1ª onda positiva : onda R.1ª onda positiva : onda R.onda negativa que sigue : onda S. onda negativa que sigue : onda S.
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
QRS:QRS: . . Se utilizan mayúsculas o minúsculas Se utilizan mayúsculas o minúsculas
en función del tamaño de dichas en función del tamaño de dichas ondas.ondas.
Cuando hay una sola onda negativa Cuando hay una sola onda negativa se denomina complejo QSse denomina complejo QS
QRS QRS
deflexión intrinsecoide:deflexión intrinsecoide: tiempo desde el inicio del QRS tiempo desde el inicio del QRS hasta el momento en que la hasta el momento en que la onda R cambia de dirección.onda R cambia de dirección.
duración normal <0,045 seg.duración normal <0,045 seg. se utiliza en el diagnóstico de la se utiliza en el diagnóstico de la hipertrofia ventricular izquierda, en hipertrofia ventricular izquierda, en la dilatación ventricular izquierda y la dilatación ventricular izquierda y en el hemibloqueo anterioren el hemibloqueo anterior
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Segmento ST:Segmento ST:
periodo periodo isoeléctricoisoeléctrico
que sigue al QRS. que sigue al QRS.
Va desde el punto J Va desde el punto J
(punto de unión del (punto de unión del
segmento ST con el segmento ST con el
QRS ) hasta el inicio QRS ) hasta el inicio
de la T de la T
Segmento STSegmento ST
Tiempo entre la Tiempo entre la despolarización despolarización total del total del ventrículo y su ventrículo y su repolarización repolarización
Mide 0,12 Mide 0,12 segundos o segundos o menos menos
Segmento STSegmento ST
En la mayoría de las derivaciones En la mayoría de las derivaciones es planoes plano
Debe estar al mismo nivel que Debe estar al mismo nivel que el segmento TP que sigue.el segmento TP que sigue.
Ascenso o depresión del STAscenso o depresión del ST: sugerente de isquemia miocárdica
Segmento STSegmento ST
Entre V1 y V3 Entre V1 y V3 presenta rápido presenta rápido ascenso y se ascenso y se fusiona con onda Tfusiona con onda T difícil de difícil de identificar.identificar.
Segmento STSegmento ST
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Onda T:Onda T: onda asimétrica, cuya 1ª onda asimétrica, cuya 1ª
mitad es una curva más gradual mitad es una curva más gradual
que la 2ª.que la 2ª.
Su orientación coincide con la del Su orientación coincide con la del
QRS. QRS.
Onda TOnda T
representa la repolarización y reposo representa la repolarización y reposo
ventricular (periodo refractario) ventricular (periodo refractario)
Dura aproximadamente 0,20 segundos Dura aproximadamente 0,20 segundos
o menos y mide 0,5 mVo menos y mide 0,5 mV
Onda TOnda T Inicio onda TInicio onda T : periodo refractario : periodo refractario efectivoefectivo
Se altera en una serie de patologías Se altera en una serie de patologías (HVI, infarto miocardio, alteración ácido (HVI, infarto miocardio, alteración ácido base, hiperkalemia) base, hiperkalemia)
Analiza unda U
acelasi sens cu unda Tvizualizare optima V3evidentiere:- hK+, cu polaritate nemodif.
- ischemie, incarc. VS din HTA, IMi, IAo negat. - ECG de repaus, U neg. stenoza TC sau IVA
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Intervalo QT:Intervalo QT: desde inicio de desde inicio de QRS hasta fin de QRS hasta fin de onda T.onda T.
De 0,2 a 0,4 De 0,2 a 0,4 segundos. segundos. Aproximadamente Aproximadamente 40% del R-R.40% del R-R.
Intervalo Q-TIntervalo Q-T
Representa toda la Representa toda la actividad actividad ventricularventricular..Depende da la frecuencia Depende da la frecuencia cardiaca:cardiaca: a mayor a mayor frecuencia, menor QT frecuencia, menor QT (repolarización se (repolarización se acorta) acorta) Se prolonga con la edad Se prolonga con la edad y algunos fármacos y algunos fármacos
INTERVALOSINTERVALOS
120-200 mseg
350-440 mseg
80-100 mseg
Fibrilatie atriala Bradicardie sinusala
Rotatie antiorara
Rotatie orara
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 de VS• formule de expunere:
1) HVS = crit. dg. clare2) 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 durata, aparut ca urmare a solicitarilor de volum si de presiune impuse miocardului VD• etiologie: incarcare de volum - DSV, Fallot, PCA (sunt stg. – dr.)
incarcare de presiune – HTP esent., HTP sec.(emfizem, TBC, bronsiectazii bilat., fibroze pulm., SMi)• fiziopatol.- balanta vectoriala VD-VS se schimba pana la predom. 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 posterioara
a vf. inimii - prin masa VD asincronism VD-VS
• consecinte ECG: - devierea ax. dreapta QRS - modif. modele epicard.
HVD moderat - hvoltaj QRS - nemodif. TADI - asincronism inversat = Hdeviatie dr.
= invers. modele epicard.
HVD concentric - Htrof. masa septala dr. – QS V5, V6, aVL, D1 - tulb. sec. faza term imag. dir. V1,V2, imag indir. V5, V6, D1, aVL
• difera asp. electrofiziol. intre HVD de orig. volemica (parietala) si cea presionala (rezistenta, concentrica)
• in HVD volemica se asoc. un grad de dilat. VD
HVD avansata
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
b) BRD masurare de TADI c) IMA postero-bazal si posterolatera
• strain: asociaza tulbur. independente celor strict de HVD
Supraincarcre de VS + VDCriteriile ECG: Criterii de voltaj pt HVS in precordiale + Hdeviatie ax spre dr. 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 WaveformECG Waveform
Electrical signal spreadsElectrical signal spreads
from the right atrium to thefrom the right atrium to the
left atrium, this is a P waveleft atrium, this is a P wave
on the diagram. This has on the diagram. This has
been known to showbeen known to show
atrium enlargementatrium enlargement
T WaveT Wave
The T wave The T wave represents the represents the recovery of the recovery of the ventriclesventricles
Inverted T wave can Inverted T wave can be a sign of coronary be a sign of coronary problemsproblems
GoalsGoals
3-Nov-083-Nov-08– Have Matlab extracting ECG waveform, develop a algorithm to Have Matlab extracting ECG waveform, develop a algorithm to
detect the QRS complexdetect the QRS complex
24-Nov-0824-Nov-08– Have Implement a neural network and integrate with the Front Have Implement a neural network and integrate with the Front
End Processor. Verity using the MIT-BIH databaseEnd Processor. Verity using the MIT-BIH database
12-Jan-0912-Jan-09– Transfer the ECG system from Matlab to C, as a real-time Transfer the ECG system from Matlab to C, as a real-time
Implementation. The neural network needs to be in C.Implementation. The neural network needs to be in C.
GoalsGoals
9-Feb-099-Feb-09– Develop hardware circuit to interact with the Develop hardware circuit to interact with the
software, thus a circuit that has a ECG sensorsoftware, thus a circuit that has a ECG sensor
9-Mar-099-Mar-09– Investigate possible extensions of the system. Investigate possible extensions of the system.
Eg. Web-based database system that could Eg. Web-based database system that could be used story cardiology records and analysisbe used story cardiology records and analysis
Health and SafetyHealth and Safety
Design of electronic circuitsDesign of electronic circuits
Hardware/software conflictsHardware/software conflicts
Testing of human subjects need approvalTesting of human subjects need approval
DESPOLARIZACIONDESPOLARIZACIONVENTRICULARVENTRICULAR
El proceso de la despolarización El proceso de la despolarización ventricular esta representado en EKG ventricular esta representado en EKG por el complejo QRS, que es la suma por el complejo QRS, que es la suma
de una secuencia de vectores de una secuencia de vectores instantáneos.instantáneos.
VECTORES QRSVECTORES QRS
DERECHA- ADELANTE
IZQUIERDA - ATRÁS
ARRIBA - ATRÁS
REPOLARIZACIONREPOLARIZACIONVENTRICULARVENTRICULAR
La repolarizacion ocurre en La repolarizacion ocurre en dirección opuesta al vector QRS, dirección opuesta al vector QRS, va desde el epicardio hacia el va desde el epicardio hacia el endocardio.endocardio.
ELECTROCARDIOGRAMAELECTROCARDIOGRAMA
1) Definiţie
2) Istoric
3) Principiu
4) Electrozi şi derivaţii
5) Analiza ECG
ELECTROZI ŞI DERIVAŢIIELECTROZI ŞI DERIVAŢII
O derivaţie este formată din doi electrozi care culeg variaţiile de potenţial electric produse în cursul ciclului cardiac
1. BIPOLAREDerivaţiile standard ale membrelor: DI, DII, DIII
2. UNIPOLAREDerivaţiile unipolare ale membrelor: aVR, aVL, aVF
Derivaţiile unipolare precordiale:V1-V6
Derivaţiile standard ale membrelorDerivaţiile standard ale membrelor
DI, DII şi DIII
descrise de Einthoven
înregistrează direcţia, amplitudinea şi durata variaţilor de voltaj în plan frontal
Rezultă prin combinarea a trei electrozi: R (plasat pe braţul drept)L (plasat pe braţul stâng)F (plasat pe gamba stângă)
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVR aVR – perpendiculară pe perpendiculară pe
DIII DIII – culege diferenţa de culege diferenţa de
potenţial dintre potenţial dintre RR (electrodul (electrodul pozitivpozitiv) şi ) şi LL şi şi FF legaţi legaţi împreună (electrodul împreună (electrodul negativnegativ))
Derivaţiile unipolare ale membrelorDerivaţiile unipolare ale membrelor
aVFaVF – perpendiculară pe DIperpendiculară pe DI– culege diferenţa de culege diferenţa de
potenţial dintre potenţial dintre FF (electrodul (electrodul pozitivpozitiv) şi ) şi RR şi şi LL legaţi legaţi împreună (electrodul împreună (electrodul negativnegativ))
Derivaţiile unipolare precordialeDerivaţiile unipolare precordiale
V1, V2, V3, V4, V5, V6V1, V2, V3, V4, V5, V6electrodul electrodul exploratorexplorator ( (pozitivpozitiv) este plasat succesiv ) este plasat succesiv pe torace în diferite zone precordiale, iar electrodul pe torace în diferite zone precordiale, iar electrodul de de referinţăreferinţă ( (negativnegativ, electrodul central , electrodul central WilsonWilson) se ) se realizează prin unirea electrozilor R, L şi Frealizează prin unirea electrozilor R, L şi Fexplorează explorează planul orizontalplanul orizontal al inimii al inimiielectrodul explorator este plasat pentru: electrodul explorator este plasat pentru:
V1V1, în spaţiul 4 intercostal, pe marginea dreaptă a sternului, în spaţiul 4 intercostal, pe marginea dreaptă a sternuluiV2V2, în spaţiul 4 intercostal, pe marginea stângă a sternului, în spaţiul 4 intercostal, pe marginea stângă a sternuluiV3V3, între V2 şi V4 , între V2 şi V4 V4V4, în spaţiul 5 intercostal, pe linia medioclaviculară, în spaţiul 5 intercostal, pe linia medioclavicularăV5V5, în spaţiul 5 intercostal, pe linia axilară anterioară, în spaţiul 5 intercostal, pe linia axilară anterioarăV6V6, în spaţiul 5 intercostal, pe linia medioaxilară, în spaţiul 5 intercostal, pe linia medioaxilară
Derivaţiile unipolare precordialeDerivaţiile unipolare precordiale
Pot fi aplicate şi derivaţii suplimentare Pot fi aplicate şi derivaţii suplimentare stângi:stângi:
V7V7, în spaţiul 5 intercostal, pe linia axilară posterioară , în spaţiul 5 intercostal, pe linia axilară posterioară stângăstângăV8V8, tot în spaţiul 5 intercostal, pe linia scapulară medie , tot în spaţiul 5 intercostal, pe linia scapulară medie stângăstângăV9V9, pe linia paravertebrală stângă, la jumătatea distanţei , pe linia paravertebrală stângă, la jumătatea distanţei dintre V8 şi coloana vertebrală.dintre V8 şi coloana vertebrală.
De asemenea pot fi utile pentru diagnosticul De asemenea pot fi utile pentru diagnosticul unui infarct miocardic de ventricul drept şi unui infarct miocardic de ventricul drept şi precordialele drepte: precordialele drepte: V3RV3R, , V4RV4R, , V5RV5R şi şi V6RV6R, , cu localizare simetrică cu cea a cu localizare simetrică cu cea a precordialelor stângiprecordialelor stângi
Unda PUnda P
reprezintă reprezintă depolarizarea atrialădepolarizarea atrială şi este: şi este:rotunjită, simetrică, rotunjită, simetrică, pozitivăpozitivă în în DII, DIII şi aVFDII, DIII şi aVF şi şi negativănegativă în în aVRaVRcu durata: 0,08-0,12 seccu durata: 0,08-0,12 secamplitudinea maximă în DII (0,25 mV)amplitudinea maximă în DII (0,25 mV)defineşte defineşte RITMUL SINUSALRITMUL SINUSAL
Intervalul PR (PQ)Intervalul PR (PQ)
cuprinde cuprinde depolarizarea atrialădepolarizarea atrială şi şi conducerea intraatrială conducerea intraatrială şi atrioventricularăşi atrioventriculară
are durata normală: 0,12-0,20 secare durata normală: 0,12-0,20 sec
se scurtează cu creşterea frecvenţei cardiace (FC)se scurtează cu creşterea frecvenţei cardiace (FC)
durata sa creşte odată cu tonusul vagaldurata sa creşte odată cu tonusul vagal
Complexul QRSComplexul QRS
semnifică semnifică depolarizarea ventricularădepolarizarea ventriculară şi este format şi este format din:din:
unda Qunda Q, prima undă , prima undă negativănegativă, reprezintă , reprezintă depolarizarea septuluidepolarizarea septului interventricularinterventricularunda Runda R, prima undă , prima undă pozitivăpozitivă, reprezintă depolarizarea simultană a , reprezintă depolarizarea simultană a ventriculului drept şi a ventriculului drept şi a regiunii apicaleregiunii apicale şi centrale a ventriculului stâng şi centrale a ventriculului stângunda Sunda S, a doua undă , a doua undă negativănegativă, este dată de depolarizarea regiunii , este dată de depolarizarea regiunii posterobazale a ventriculului stângposterobazale a ventriculului stâng
Complexul QRSComplexul QRS
în cazul prezenţei mai multor unde pozitive, prima dintre în cazul prezenţei mai multor unde pozitive, prima dintre ele se notează R, iar următoarele unde pozitive: R΄, R΄΄ etc.ele se notează R, iar următoarele unde pozitive: R΄, R΄΄ etc.
dacă complexul depolarizării ventriculare este format doar dacă complexul depolarizării ventriculare este format doar dintr-o deflexiune negativă, se numeşte QSdintr-o deflexiune negativă, se numeşte QS
durata: 0,08-0,10 secdurata: 0,08-0,10 sec
Complexul QRSComplexul QRS
amplitudinea: minimum 5 mm in derivaţiile standard şi amplitudinea: minimum 5 mm in derivaţiile standard şi minimum 10 mm în precordiale. Sub aceste valori se minimum 10 mm în precordiale. Sub aceste valori se consideră microvoltaj şi peste aceste valori macrovoltaj. consideră microvoltaj şi peste aceste valori macrovoltaj. Deflexiunile de peste 3 mm sunt notate cu litere mari (Q; Deflexiunile de peste 3 mm sunt notate cu litere mari (Q; R; S), iar cele sub 3 mm cu litere mici (q, r, s)R; S), iar cele sub 3 mm cu litere mici (q, r, s)
Segmentul STSegmentul ST
reprezintă porţiunea iniţială, lentă a reprezintă porţiunea iniţială, lentă a repolarizării repolarizării ventriculareventriculare
începe la punctul J (“junction”), situat la limita dintre unda S şi începe la punctul J (“junction”), situat la limita dintre unda S şi segmentul ST, trebuie să fie situat pe linia izoelectrică sau la segmentul ST, trebuie să fie situat pe linia izoelectrică sau la 1mm deasupra sau dedesubt de aceasta 1mm deasupra sau dedesubt de aceasta
este este orizontalorizontal şi şi izoelectricizoelectric
Unda TUnda T
reprezintă porţiunea terminală, rapidă a reprezintă porţiunea terminală, rapidă a repolarizării repolarizării ventriculareventriculare
este rotunjită, este rotunjită, asimetricăasimetrică, cu panta ascendentă mai lentă şi cea , cu panta ascendentă mai lentă şi cea descendentă mai rapidădescendentă mai rapidă
concordantă ca sens cu complexul QRSconcordantă ca sens cu complexul QRS
amplitudinea de aproximativ 1/3 din cea a complexului QRSamplitudinea de aproximativ 1/3 din cea a complexului QRS
Intervalul QTIntervalul QT
defineşte durata totală a defineşte durata totală a depolarizării şi depolarizării şi repolarizării ventricularerepolarizării ventriculare
variază invers proporţional cu frecvenţa cardiacăvariază invers proporţional cu frecvenţa cardiacăvalorile sale se pot corecta în funcţie de frecvenţa valorile sale se pot corecta în funcţie de frecvenţa cardiacă (QTc), conform cardiacă (QTc), conform formulei Bazettformulei Bazett: QTc = QT/√RR, : QTc = QT/√RR, unde RR este intervalul RR în msunde RR este intervalul RR în mslimita superioară a intervalului QTc este de 0,45 seclimita superioară a intervalului QTc este de 0,45 sec
Determinarea axului electric al inimiiDeterminarea axului electric al inimii
Axul electric Axul electric reprezintă reprezintă direcţia procesului de activare cardiacădirecţia procesului de activare cardiacă proiectat în derivaţiile membrelorproiectat în derivaţiile membrelorrezultă din sumarea în plan frontal a vectorilor electrici rezultă din sumarea în plan frontal a vectorilor electrici generaţi în cursul depolarizării şi repolarizării atriilor şi generaţi în cursul depolarizării şi repolarizării atriilor şi ventriculilor şi se reprezintă sub forma unui vector în ventriculilor şi se reprezintă sub forma unui vector în sistemul de referinţă hexaxialsistemul de referinţă hexaxial
De obicei, se determină De obicei, se determină axul depolarizării axul depolarizării ventriculare (AQRS)ventriculare (AQRS) care poate fi: care poate fi:
normalnormal: între : între –30 şi +110–30 şi +110 grade gradedeviat patologic la deviat patologic la stângastânga: între : între –30 şi –90 grade–30 şi –90 gradedeviat patologic la deviat patologic la dreaptadreapta: între : între +110 şi +180 grade+110 şi +180 grade
Determinarea axului electric al inimiiDeterminarea axului electric al inimii
Pentru a calcula AQRS:Pentru a calcula AQRS:se determină se determină suma algebricăsuma algebrică a deflexiunii a deflexiunii maxime pozitive cu deflexiunea maximă maxime pozitive cu deflexiunea maximă negativă, în două din derivaţiile planului frontal negativă, în două din derivaţiile planului frontal care sunt perpendicularecare sunt perpendicularevaloarea obţinută se reprezintă ca valoarea obţinută se reprezintă ca vectorvector în în sistemul hexaxial, ţinând seama de polaritatesistemul hexaxial, ţinând seama de polaritatese trasează perpendiculare din vârful vectorilor se trasează perpendiculare din vârful vectorilor reprezentaţireprezentaţise uneşte centrul sistemului hexaxial cu se uneşte centrul sistemului hexaxial cu punctual de intersecţie a celor două punctual de intersecţie a celor două perpendiculare, rezultând AQRSperpendiculare, rezultând AQRS
Determinarea axului electric al inimiiDeterminarea axului electric al inimii
Metode rapide pentru stabilirea axului Metode rapide pentru stabilirea axului electric al inimii:electric al inimii:
se observă în care derivaţie a planului frontal, se observă în care derivaţie a planului frontal, amplitudinea QRS este maximăamplitudinea QRS este maximă; derivaţia ; derivaţia respectivă corespunde poziţiei axului electricrespectivă corespunde poziţiei axului electric– Exemple: Exemple:
S maxim în aVF → AQRS la -90 gradeS maxim în aVF → AQRS la -90 grade
R maxim în aVL → AQRS la -30 gradeR maxim în aVL → AQRS la -30 grade
Determinarea axului electric al inimiiDeterminarea axului electric al inimii
Metode rapide pentru stabilirea axului Metode rapide pentru stabilirea axului electric al inimii:electric al inimii:
aspectul complexului QRS din derivaţiile DI aspectul complexului QRS din derivaţiile DI sau DIIIsau DIII::
aspect RI RIII → AQRS normalaspect RI RIII → AQRS normal
aspect RI SIII → AQRS deviat patologic la aspect RI SIII → AQRS deviat patologic la stângastânga
aspect SI RIII → AQRS deviat patologic la aspect SI RIII → AQRS deviat patologic la dreapta.dreapta.
Normal Axis = -30 to +120
RAD =+120 to +180
LAD = -30 to -90
No Man’s Land Axis = -90 to +- 180
Determinarea axului electric al inimiiDeterminarea axului electric al inimii
LAD– Anterior Hemiblock– Inferior MI– WPW – right pathway– Emphysema
RAD– Children, thin adults– RVH– Chronic Lung Disease– WPW – left pathway– Pulmonary emboli– Posterior Hemiblock
No Man’s Land– Emphysema– Hyperkalemia– Lead Transposition– V-Tach
Determinarea frecvenţei cardiaceDeterminarea frecvenţei cardiace
Frecvenţa cardiacă (FC) normală de Frecvenţa cardiacă (FC) normală de repaus este de: 60-100/minutrepaus este de: 60-100/minut
Se ţine seama de următoarele principii:Se ţine seama de următoarele principii:viteza standard de derulare a hârtiei este de 25 viteza standard de derulare a hârtiei este de 25 mm/secmm/sec
FC se exprimă în cicluri/minutFC se exprimă în cicluri/minut
se verifică dacă frecvenţa atrială este egală cu se verifică dacă frecvenţa atrială este egală cu cea ventricularăcea ventriculară
Determinarea frecvenţei cardiaceDeterminarea frecvenţei cardiace
FC poate fi determinată cu ajutorul ecuaţiei: FC poate fi determinată cu ajutorul ecuaţiei:
1 secundă................25mm1 secundă................25mm
60 secunde..............x60 secunde..............x
(1 minut)(1 minut)
x = 60x25 = 1500mm/minut.x = 60x25 = 1500mm/minut.
FC = 1500/intervalul R-R în mmFC = 1500/intervalul R-R în mm
Determinarea rapidă a frecvenţei cardiaceDeterminarea rapidă a frecvenţei cardiace
Se poate face pe baza următoarelor Se poate face pe baza următoarelor principii:principii:
hârtia ECG este marcată prin linii subţiri în hârtia ECG este marcată prin linii subţiri în pătrate mici cu latura de 1mm şi linii groase în pătrate mici cu latura de 1mm şi linii groase în pătrate mari cu latura de 5 mmpătrate mari cu latura de 5 mm
la viteza de 25 mm/sec, la 1 minut (60 secunde) la viteza de 25 mm/sec, la 1 minut (60 secunde) corespund 1500 mmcorespund 1500 mm
Determinarea rapidă a frecvenţei cardiaceDeterminarea rapidă a frecvenţei cardiace
– se caută pe ECG o undă R suprapusă peste o linie se caută pe ECG o undă R suprapusă peste o linie groasă şi se numără liniile groase după care groasă şi se numără liniile groase după care apare următoarea undă R pentru a aprecia FC apare următoarea undă R pentru a aprecia FC astfel: astfel: 300300, , 150150, , 100100, , 7575, , 6060, , 5050
Interpretación del ECGInterpretación del ECGFrecuencia cardiacaFrecuencia cardiaca : : se se determina dividiendo 300 por el nº determina dividiendo 300 por el nº de cuadrados grandes entre dos de cuadrados grandes entre dos QRS seguidosQRS seguidos . .
Interpretación del ECGInterpretación del ECG
Frecuencia cardiacaFrecuencia cardiaca en trazado en trazado irregularirregular::. Tomar un trazado de 25 cms . Tomar un trazado de 25 cms (10 segundos), contar el nº de intervalos (10 segundos), contar el nº de intervalos entre los QRS en ese tiempo y entre los QRS en ese tiempo y multiplicarlo por 6 multiplicarlo por 6
Ritmo anormal del NSARitmo anormal del NSA
TaquicardiaTaquicardia: : frecuencia mayor o igual a frecuencia mayor o igual a
100 latidos / minuto100 latidos / minuto
Ritmo anormal del NSARitmo anormal del NSA
BradicardiaBradicardia: frecuencia : frecuencia menor o igual a 60 latidos / menor o igual a 60 latidos / minutominuto
Vector neto de despolarización Vector neto de despolarización En las distintas derivaciones la amplitud En las distintas derivaciones la amplitud de los potenciales medidos y graficados de los potenciales medidos y graficados en el papel depende de la orientación en el papel depende de la orientación del electrodo positivo en relación al del electrodo positivo en relación al vector eléctrico neto .vector eléctrico neto .
Vector neto de despolarización QRSVector neto de despolarización QRS Sistema Sistema hexaxialhexaxial se usa se usa para para determinar el determinar el potencial que potencial que registrará el registrará el ECG ECG en cada en cada una de las una de las derivacionesderivaciones para un vector para un vector dado dado
Vectores netos de despolarizaciónVectores netos de despolarización
Corazón despolarizado Corazón despolarizado parcialmente.parcialmente.
A: vector medio de despolarizaciónA: vector medio de despolarización del QRS:del QRS: tiene una dirección y tiene una dirección y largo, que determina el voltaje del largo, que determina el voltaje del potencial generado.potencial generado. (por ejemplo (por ejemplo 55º y 2mV)55º y 2mV)
Para determinar la magnitud del Para determinar la magnitud del voltaje del voltaje del vector A en DIvector A en DI se traza una se traza una línea perpendicular al eje de DI desde línea perpendicular al eje de DI desde la punta de A y dibujamos el vector la punta de A y dibujamos el vector proyectado B proyectado B
Vectores netos de despolarizaciónVectores netos de despolarización
B apunta al polo + de DI: voltaje en B apunta al polo + de DI: voltaje en esa derivación es + y esa derivación es + y aproximadamente la mitad de Aaproximadamente la mitad de A
Vectores netos de despolarizaciónVectores netos de despolarización
Vectores netos de Vectores netos de despolarización: QRSdespolarización: QRS
B: proyección de A en DIB: proyección de A en DI
D: proyección de A en DIIID: proyección de A en DIII C: proyección de A en DIIC: proyección de A en DII
0,01 seg 0,02 seg
0,05 seg0,035 seg
0,06 seg
Vectores netos de Vectores netos de despolarización : despolarización : onda Ponda P
Vectores netos deVectores netos de despolarización : onda Tdespolarización : onda T
Se debe medir la duración y Se debe medir la duración y voltaje de los complejos y ondasvoltaje de los complejos y ondas
Se debe medir la duración y Se debe medir la duración y voltaje de los complejos y ondasvoltaje de los complejos y ondas
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
DuraciónDuración: 0,08 a 0,10 s: 0,08 a 0,10 s (< (< 0,12 s o < 2,5 mm)0,12 s o < 2,5 mm)
Altura:Altura: < de 0,25 mV (< 2,5 < de 0,25 mV (< 2,5 mm)mm)
Onda POnda P
Incluye tiempo de despolarización Incluye tiempo de despolarización auricular y de conducción auricular y de conducción auriculoventricular y del sistema auriculoventricular y del sistema His- PurkinjeHis- Purkinje
Intervalo PRIntervalo PR
Intervalo PR Intervalo PR
Se mide desde el Se mide desde el inicio de la onda P inicio de la onda P hasta el inicio del hasta el inicio del complejo QRS. complejo QRS.
Duración: desde Duración: desde inicio de la P al inicio de la P al inicio del QRS, va inicio del QRS, va de 0,12 a 0,20 de 0,12 a 0,20 segseg
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Complejo Complejo QRSQRS::
despolarización despolarización ventricular.ventricular.
Duración:Duración:
0,06 a 0,10 0,06 a 0,10 segundossegundos
QRS: presenta diversas morfologías en QRS: presenta diversas morfologías en diferentes derivacionesdiferentes derivaciones
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
QRS:QRS: 1ª onda negativa : onda Q.1ª onda negativa : onda Q.1ª onda positiva : onda R.1ª onda positiva : onda R.onda negativa que sigue : onda S. onda negativa que sigue : onda S.
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
QRS:QRS: . . Se utilizan mayúsculas o minúsculas Se utilizan mayúsculas o minúsculas
en función del tamaño de dichas en función del tamaño de dichas ondas.ondas.
Cuando hay una sola onda negativa Cuando hay una sola onda negativa se denomina complejo QSse denomina complejo QS
QRS QRS
deflexión intrinsecoide:deflexión intrinsecoide: tiempo desde el inicio del QRS tiempo desde el inicio del QRS hasta el momento en que la hasta el momento en que la onda R cambia de dirección.onda R cambia de dirección.
duración normal <0,045 seg.duración normal <0,045 seg. se utiliza en el diagnóstico de la se utiliza en el diagnóstico de la hipertrofia ventricular izquierda, en hipertrofia ventricular izquierda, en la dilatación ventricular izquierda y la dilatación ventricular izquierda y en el hemibloqueo anterioren el hemibloqueo anterior
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Segmento ST:Segmento ST:
periodo periodo isoeléctricoisoeléctrico
que sigue al QRS. que sigue al QRS.
Va desde el punto J Va desde el punto J
(punto de unión del (punto de unión del
segmento ST con el segmento ST con el
QRS ) hasta el inicio QRS ) hasta el inicio
de la T de la T
Segmento STSegmento ST
Tiempo entre la Tiempo entre la despolarización despolarización total del total del ventrículo y su ventrículo y su repolarización repolarización
Mide 0,12 Mide 0,12 segundos o segundos o menos menos
Segmento STSegmento ST
En la mayoría de las derivaciones En la mayoría de las derivaciones es planoes plano
Debe estar al mismo nivel que Debe estar al mismo nivel que el segmento TP que sigue.el segmento TP que sigue.
Ascenso o depresión del STAscenso o depresión del ST: sugerente de isquemia miocárdica
Segmento STSegmento ST
Entre V1 y V3 Entre V1 y V3 presenta rápido presenta rápido ascenso y se ascenso y se fusiona con onda Tfusiona con onda T difícil de difícil de identificar.identificar.
Segmento STSegmento ST
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Onda T:Onda T: onda asimétrica, cuya 1ª onda asimétrica, cuya 1ª
mitad es una curva más gradual mitad es una curva más gradual
que la 2ª.que la 2ª.
Su orientación coincide con la del Su orientación coincide con la del
QRS. QRS.
Onda TOnda T
representa la repolarización y reposo representa la repolarización y reposo
ventricular (periodo refractario) ventricular (periodo refractario)
Dura aproximadamente 0,20 segundos Dura aproximadamente 0,20 segundos
o menos y mide 0,5 mVo menos y mide 0,5 mV
Onda TOnda T Inicio onda TInicio onda T : periodo refractario : periodo refractario efectivoefectivo
Se altera en una serie de patologías Se altera en una serie de patologías (HVI, infarto miocardio, alteración ácido (HVI, infarto miocardio, alteración ácido base, hiperkalemia) base, hiperkalemia)
Valores normales de voltaje y Valores normales de voltaje y duraciónduración
Intervalo QT:Intervalo QT: desde inicio de desde inicio de QRS hasta fin de QRS hasta fin de onda T.onda T.
De 0,2 a 0,4 De 0,2 a 0,4 segundos. segundos. Aproximadamente Aproximadamente 40% del R-R.40% del R-R.
Intervalo Q-TIntervalo Q-T
Representa toda la Representa toda la actividad actividad ventricularventricular..Depende da la frecuencia Depende da la frecuencia cardiaca:cardiaca: a mayor a mayor frecuencia, menor QT frecuencia, menor QT (repolarización se (repolarización se acorta) acorta) Se prolonga con la edad Se prolonga con la edad y algunos fármacos y algunos fármacos
En aVL el QRS es positivo: el eje se En aVL el QRS es positivo: el eje se encuentra a - 30º. encuentra a - 30º.
Si aVL fuera negativo, el eje Si aVL fuera negativo, el eje estaría a + 150º estaría a + 150º
Desviación izquierda por HVIDesviación izquierda por HVI
Desviación derecha por HVDDesviación derecha por HVD
Bloqueo rama izquierdoBloqueo rama izquierdo
BRDBRD
Utilidad clínicaUtilidad clínica
ECG anormalECG anormal
Ritmos anormales por Ritmos anormales por bloqueos de la bloqueos de la
conducción conducción
Bloqueo sinusalBloqueo sinusal
El ECG se salta un latidoEl ECG se salta un latido
Bloqueo sinusalBloqueo sinusal
Los complejos antes y Los complejos antes y después del paro sinusal son después del paro sinusal son normales normales
Bloqueo sinusalBloqueo sinusal
Si bloqueo permaneceSi bloqueo permanece: NAV : NAV inicia despolarización inicia despolarización
Ritmo no sinusal (no hay P)Ritmo no sinusal (no hay P)
Frecuencia lenta Frecuencia lenta
Complejos QRS-T normales Complejos QRS-T normales
Bloqueo sinusal con ritmo del Bloqueo sinusal con ritmo del nódulo AVnódulo AV
2. Bloqueo auriculoventricular2. Bloqueo auriculoventricular
NAV: único paso entre As y Vs.NAV: único paso entre As y Vs. Causas:Causas:
1.1. Isquemia del NAV o Haz de HisIsquemia del NAV o Haz de His
2.2. Inflamacion NAV o Haz de His Inflamacion NAV o Haz de His (miocarditis) (miocarditis)
3.3. Compresión externa del NAV o Compresión externa del NAV o Haz de HizHaz de Hiz
Bloqueo AVBloqueo AV
Tipos:Tipos:
1.1. Bloqueo AV de primer gradoBloqueo AV de primer grado
2.2. Bloqueo AV de 2º grado Bloqueo AV de 2º grado
3.3. Bloqueo AV de tercer grado Bloqueo AV de tercer grado
Bloqueo auriculoventricularBloqueo auriculoventricular
La conducción por el NAV está La conducción por el NAV está retrasada, pero el impulso se retrasada, pero el impulso se propaga y excita los ventrículos propaga y excita los ventrículos de manera normal.de manera normal.
Existe una onda P por cada Existe una onda P por cada complejo QRS. complejo QRS.
Bloqueo AV de primer Bloqueo AV de primer gradogrado
Bloqueo AV de primer Bloqueo AV de primer grado grado
Ritmo sinusal normal Ritmo sinusal normal
Onda P normalOnda P normal
Complejo QRS normales Complejo QRS normales
Prolongación del intervalo PRProlongación del intervalo PR : : mayor a 0,20 segundos.mayor a 0,20 segundos.
Bloqueo AV de 2º gradoBloqueo AV de 2º grado
Conducción eléctrica por NAV lenta.Conducción eléctrica por NAV lenta.
Algunos impulsos no se conducenAlgunos impulsos no se conducen . .
Onda P sin QRSOnda P sin QRS
Bloqueo AV de 2º grado Bloqueo AV de 2º grado tipo Mobitztipo Mobitz I I
impulsos conducidos con un intervalo PR impulsos conducidos con un intervalo PR variable, generalmente tipo variable, generalmente tipo WenckebachWenckebach: : Los intervalos PR alargan Los intervalos PR alargan progresivamente hasta que un impulso progresivamente hasta que un impulso no se conduce. no se conduce.
El latido que no se conduce está entre El latido que no se conduce está entre dos ondas P.dos ondas P.
Los intervalos RR son cada vez más Los intervalos RR son cada vez más cortos hasta que un impulso no se cortos hasta que un impulso no se conduceconduce
Bloqueo AV de 2º grado Bloqueo AV de 2º grado tipo Mobitztipo Mobitz I I
Bloqueo AV de 2º grado Bloqueo AV de 2º grado tipo Mobitztipo Mobitz II II
ondas P no conducidas sin que haya un ondas P no conducidas sin que haya un alargamiento del intervalo PR.alargamiento del intervalo PR.
Intervalos PR constantes Intervalos PR constantes
No se conducen 2 o más ondas P: existe No se conducen 2 o más ondas P: existe relación ondas P / QRS (2:1, 3:1, 4:1)relación ondas P / QRS (2:1, 3:1, 4:1)
Precursor frecuente del bloqueo Precursor frecuente del bloqueo AV completo, especialmente si AV completo, especialmente si se acompaña de bloqueos de se acompaña de bloqueos de rama. rama.
Se asocia a isquemia Se asocia a isquemia
Bloqueo AV de 2º grado Bloqueo AV de 2º grado tipo Mobitztipo Mobitz II II
Bloqueo AV de tercer grado Bloqueo AV de tercer grado
Lesión severa al NAV: Lesión severa al NAV: ningún ningún impulso auricular llega a los impulso auricular llega a los ventrículosventrículos : aurículas y : aurículas y ventrículos están controlados por ventrículos están controlados por marcapasos independientesmarcapasos independientes
Bloqueo AV de tercer grado Bloqueo AV de tercer grado Ondas P normales . PR no es medible Ondas P normales . PR no es medible
no existe ninguna relación entre las no existe ninguna relación entre las
ondas P y los complejos QRS: ondas P y los complejos QRS: disociación disociación
auriculoventricular completaauriculoventricular completa
frecuencia de ondas P generalmente frecuencia de ondas P generalmente
mayor a la de QRS mayor a la de QRS
Despolarización ventricular es por Despolarización ventricular es por marcapasos ectópicos : marcapasos ectópicos :
has de Hiz:has de Hiz: 40 a 55 /minuto. QRS 40 a 55 /minuto. QRS normalesnormales
VentricularVentricular: 20 a 40 /minuto. QRS : 20 a 40 /minuto. QRS anchos anchos
Frecuencia QRS lenta (menor a Frecuencia QRS lenta (menor a 40/minuto) regular.40/minuto) regular.
Bloqueo AV de tercer gradoBloqueo AV de tercer grado
Bloqueo AV completoBloqueo AV completo
Ritmo de la unión (Has de Hiz)
Ritmo ventricular (Has de Hiz)
3. Bloqueos de rama3. Bloqueos de rama El haz de His se bifurca en las ramas derecha El haz de His se bifurca en las ramas derecha
e izquierda. Ambas ramas bajan a cada lado e izquierda. Ambas ramas bajan a cada lado
del tabique interventricular.del tabique interventricular.
Justo después de su inicio la rama izquierda Justo después de su inicio la rama izquierda
se divide en una rama anterior y otra se divide en una rama anterior y otra
posterior. posterior.
En cualquiera de estas estructuras En cualquiera de estas estructuras
puede bloquearse la conducción del puede bloquearse la conducción del
estimulo estimulo
Conducción normalConducción normal: la activación : la activación de los ventrículos se inicia en el de los ventrículos se inicia en el lado izquierdo del tabique lado izquierdo del tabique interventricular y se propaga interventricular y se propaga hacia la derecha.hacia la derecha.
3. Bloqueos de rama3. Bloqueos de rama
Bloqueo rama derecha Bloqueo rama derecha
Puede verse en Puede verse en personas sanaspersonas sanas
Se retrasa Se retrasa despolarización VDdespolarización VD
VI despolarización VI despolarización normal: 1ª mitad normal: 1ª mitad QRS normal .QRS normal .
Despolarización es a través de Despolarización es a través de tejido no especializado.tejido no especializado.
QRS ancho por mayor tiempo QRS ancho por mayor tiempo de despolarización de despolarización
Diagnóstico:Diagnóstico:
QRS QRS >> o = 0,12 o = 0,12 seg.seg.
2ª onda R en V1 o 2ª onda R en V1 o V2V2
Ondas S anchas Ondas S anchas en DI, V5 y V6en DI, V5 y V6
Depresión Depresión segmento ST e segmento ST e inversión onda T inversión onda T en precordiales en precordiales derechas derechas
Bloqueo rama izquierdaBloqueo rama izquierda
Se asocia a enfermedad coronaria, Se asocia a enfermedad coronaria,
a HTA o miocardiopatia dilatada.a HTA o miocardiopatia dilatada.
Rama izquierda irrigada por Rama izquierda irrigada por
arteria descendente anterior arteria descendente anterior
(rama coronaria izquierda) y (rama coronaria izquierda) y
coronaria derecha.coronaria derecha.
2-4% pacientes con IAM lo tienen 2-4% pacientes con IAM lo tienen
Bloqueo rama izquierdaBloqueo rama izquierda
Normalmente Normalmente despolarización despolarización va de izquierda a va de izquierda a derecha.derecha.
En BRI va de En BRI va de derecha a derecha a izquierda izquierda
vector del segmento vector del segmento ST y de la onda T es ST y de la onda T es la opuesta a la del la opuesta a la del QRSQRS
• Despolarización es a través de Despolarización es a través de tejido no especializado.tejido no especializado.
• QRS ancho por mayor tiempo QRS ancho por mayor tiempo de despolarización de despolarización
Diagnóstico Diagnóstico Complejos QRS de Complejos QRS de 0,12 seg o más.0,12 seg o más.
Pérdida de la onda Q Pérdida de la onda Q septal en DI V5 y V6 .septal en DI V5 y V6 .
ondas R dentadas ondas R dentadas (con una muesca en (con una muesca en la zona intermedia la zona intermedia del complejo QRS) en del complejo QRS) en DI, aVL, V5 y V6.DI, aVL, V5 y V6.
S profunda en S profunda en precordiales precordiales derechas derechas
BCRIBCRI
ST y onda T : ST y onda T : deflexión deflexión opuesta al QRSopuesta al QRS
infradesnivel infradesnivel ST y T ST y T negativa en DI, negativa en DI, aVL y V6.aVL y V6.
Lo contrario en Lo contrario en V1, V2 y V3 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 heart’s 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”
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
QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal
Atrial Escape Beat
Recognizing and Naming Beats & Rhythms
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
Junctional Escape BeatQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal
Recognizing and Naming Beats & Rhythms
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
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
Ventricular Escape Beat
there is no p wave, indicating that the beat did not originate anywhere in the atria
Recognizing and Naming Beats & Rhythms
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
Recognizing and Naming Beats & Rhythms
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
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac Conduction
Tissue
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
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Premature Beat Impulse
Cardiac Conduction
Tissue
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
Repolarizing Tissue (long refractory period)
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
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
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction
Tissue
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
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
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction
Tissue
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Atrial Re-entry• atrial tachycardia• atrial fibrillation• atrial flutter
Atrio-Ventricular Re-entry• Wolf Parkinson White• supraventricular tachycardia
Ventricular Re-entry• ventricular tachycardia
Atrio-Ventricular Nodal Re-entry• supraventricular tachycardia
Re-entry Circuits as Ectopic Foci and Arrhythmia Generators
Recognizing and Naming Beats & Rhythms
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
Recognizing and Naming Beats & Rhythms
Premature Ventricular Contractions (PVC’s, VPB’s, 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
• PVC’s are sometimes described by lay people as “skipped heart beats”
M ultifoca l P V C 's
C om pensa to ry pausea fte r the occu rance o f a P V C
R on T phenom em on
Recognizing and Naming Beats & Rhythms
Characteristics of PVC's • PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle• Every other beat being a PVC (bigeminy) may indicate coronary artery disease• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s
Interpolated PVC – note the sinus rhythm is undisturbed
The classic PVC – note the compensatory pause
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 • Ventricular Fibrillation
Recognizing and Naming Beats & Rhythms
sinus beatsUnconverted V-tach r V-fib
V-tach
“R on T phenomenon”
time
The sooner defibrillation takes place, the increased likelihood of survival
Recognizing and Naming Beats & Rhythms
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 p-wave in front of PVC and the PVC is narrower than the other PVC’s – 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.
Recognizing and Naming Beats & Rhythms
Premature Atrial Contractions (PAC’s):
• 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
• PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)
• PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco
• PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy
• PAC’s may also precede PSVT
PACNon conducted PAC Non conducted PAC
distorting a T-wave
Premature Junctional Contractions (PJC’s):
• 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
• PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm
Recognizing and Naming Beats & Rhythms
PJC
Recognizing and Naming Beats & Rhythms
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 SVT’s
• 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
Recognizing and Naming Beats & Rhythms
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, blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective)
Note IRREGULAR rhythm in the tachycardia
Note different P-wave morphologies when the tachycardia begins
Recognizing and Naming Beats & Rhythms
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
Note REGULAR rhythm in the tachycardiaRhythm usually begins
with PAC
ARRHYTHMIAARRHYTHMIA
Edited by Yingmin ChenEdited by Yingmin Chen
Definition of Arrhythmia:Definition of Arrhythmia:
The The Origin, Rate, Rhythm, Conduct Origin, Rate, Rhythm, Conduct velocity and sequencevelocity and sequence of heart of heart activation are activation are abnormallyabnormally..
Anatomy of the conducting system
Pathogenesis and Inducement Pathogenesis and Inducement of Arrhythmia of Arrhythmia
Some physical conditionSome physical condition
Pathological heart diseasePathological heart disease
Other system disease Other system disease
Electrolyte disturbance and acid-base Electrolyte disturbance and acid-base imbalanceimbalance
Physical and chemical factors or Physical and chemical factors or toxicosistoxicosis
Mechanism of ArrhythmiaMechanism of Arrhythmia
Abnormal heart pulse formationAbnormal heart pulse formation1.1. Sinus pulseSinus pulse2.2. Ectopic pulseEctopic pulse3.3. Triggered activityTriggered activity
Abnormal heart pulse Abnormal heart pulse conductionconduction
1.1. ReentryReentry2.2. Conduct blockConduct block
Classification of ArrhythmiaClassification of ArrhythmiaAbnormal heart pulse formationAbnormal heart pulse formation
1.1. Sinus arrhythmiaSinus arrhythmia2.2. Atrial arrhythmiaAtrial arrhythmia3.3. Atrioventricular junctional arrhythmiaAtrioventricular junctional arrhythmia4.4. Ventricular arrhythmiaVentricular arrhythmia
Abnormal heart pulse conductionAbnormal heart pulse conduction1.1. Sinus-atrial blockSinus-atrial block2.2. Intra-atrial blockIntra-atrial block3.3. Atrio-ventricular blockAtrio-ventricular block4.4. Intra-ventricular blockIntra-ventricular block
Abnormal heart pulse formation and Abnormal heart pulse formation and conductionconduction
Diagnosis of ArrhythmiaDiagnosis of Arrhythmia
Medical historyMedical history
Physical examinationPhysical examination
Laboratory testLaboratory test
Therapy PrincipalTherapy Principal
Pathogenesis therapyPathogenesis therapy
Stop the arrhythmia immediately if the Stop the arrhythmia immediately if the hemodynamic was unstablehemodynamic was unstable
Individual therapyIndividual therapy
Anti-arrhythmia AgentsAnti-arrhythmia Agents
Anti-tachycardia agentsAnti-tachycardia agents
Anti-bradycardia agentsAnti-bradycardia agents
Anti-tachycardia agentsAnti-tachycardia agents
Modified Vaugham Williams Modified Vaugham Williams classificationclassification
1.1. I class: Natrium channel blockerI class: Natrium channel blocker
2.2. II class: II class: ß-receptor blockerß-receptor blocker
3.3. III class: Potassium channel blockerIII class: Potassium channel blocker
4.4. IV class: Calcium channel blockerIV class: Calcium channel blocker
5.5. Others: Adenosine, DigitalOthers: Adenosine, Digital
Anti-bradycardia agentsAnti-bradycardia agents
1.1. ß-adrenic receptor activatorß-adrenic receptor activator
2.2. M-M-cholinergic receptor blockercholinergic receptor blocker
3.3. Non-specific activatorNon-specific activator
Clinical usageClinical usage
Anti-tachycardia agents:Anti-tachycardia agents: Ia class: Less use in clinicIa class: Less use in clinic
1.1. GuinidineGuinidine
2.2. ProcainamideProcainamide
3.3. Disopyramide: Disopyramide: Side effect: like Side effect: like M-M-cholinergic receptor blockercholinergic receptor blocker
Anti-tachycardia agents:Anti-tachycardia agents: Ib class: Perfect to ventricular Ib class: Perfect to ventricular
tachyarrhythmiatachyarrhythmia
1. Lidocaine1. Lidocaine
2. Mexiletine2. Mexiletine
Anti-tachycardia agents:Anti-tachycardia agents: Ic class: Can be used in ventricular Ic class: Can be used in ventricular
and/or supra-ventricular tachycardia and/or supra-ventricular tachycardia and extrasystole. and extrasystole.
1. Moricizine1. Moricizine
2. Propafenone2. Propafenone
Anti-tachycardia agents:Anti-tachycardia agents:
II class: ß-receptor blockerII class: ß-receptor blocker1.1. Propranolol:Propranolol: Non-selective Non-selective
2.2. Metoprolol:Metoprolol: Selective Selective ßß11-receptor -receptor
blocker, Perfect to hypertension blocker, Perfect to hypertension and coronary artery disease and coronary artery disease patients associated with patients associated with tachyarrhythmia. tachyarrhythmia.
Anti-tachycardia agents:Anti-tachycardia agents:
III class: Potassium channel blocker, III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent.extend-spectrum anti-arrhythmia agent.
Amioarone: Perfect to coronary artery Amioarone: Perfect to coronary artery disease and heart failure patientsdisease and heart failure patients
Sotalol: Has ß-blocker effectSotalol: Has ß-blocker effect
BretyliumBretylium
Anti-tachycardia agents:Anti-tachycardia agents:
IV class: be used in supraventricular IV class: be used in supraventricular tachycardiatachycardia
1.1. VerapamilVerapamil
2.2. DiltiazemDiltiazem
Others:Others:
Adenosine: be used in Adenosine: be used in supraventricular tachycardiasupraventricular tachycardia
Anti-bradycardia agentsAnti-bradycardia agents
IsoprenalineIsoprenaline
EpinephrineEpinephrine
AtropineAtropine
AminophyllineAminophylline
Proarrhythmia effect of Proarrhythmia effect of antiarrhythmia agentsantiarrhythmia agents
Ia, Ic class: Prolong QT interval, will Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery cause VT or VF in coronary artery disease and heart failure patientsdisease and heart failure patients
III class: Like Ia, Ic class agentsIII class: Like Ia, Ic class agents
II, IV class: BradycardiaII, IV class: Bradycardia
Non-drug therapyNon-drug therapy
Cardioversion: For tachycardia especially Cardioversion: For tachycardia especially hemodynamic unstable patienthemodynamic unstable patientRadiofrequency catheter ablation (RFCA): Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, For those tachycardia patients (SVT, VT, AF, AFL)AF, AFL)Artificial cardiac pacing: For bradycardia, Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular heart failure and malignant ventricular arrhythmia patients.arrhythmia patients.
Sinus ArrhythmiaSinus Arrhythmia
Sinus tachycardiaSinus tachycardia Sinus rate > 100 beats/min (100-180)Sinus rate > 100 beats/min (100-180)
Causes:Causes:
1.1. Some physical condition: exercise, Some physical condition: exercise, anxiety, exciting, alcohol, coffeeanxiety, exciting, alcohol, coffee
2.2. Some disease: fever, Some disease: fever, hyperthyroidism, anemia, myocarditis hyperthyroidism, anemia, myocarditis
3.3. Some drugs: Atropine, Isoprenaline Some drugs: Atropine, Isoprenaline
Needn’t therapyNeedn’t therapy
SinusSinus BradycardiaBradycardiaSinus rate < 60 beats/min Sinus rate < 60 beats/min
Normal variant in many normal and older peopleNormal variant in many normal and older people
Causes:Causes: Trained athletes, during sleep, drugs Trained athletes, during sleep, drugs ((ß-blockerß-blocker) , Hypothyriodism, CAD or SSS) , Hypothyriodism, CAD or SSS
Symptoms:Symptoms:
1.1. Most patients have no symptoms.Most patients have no symptoms.
2.2. Severe bradycardia may cause dizziness, Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope. fatigue, palpitation, even syncope.
Needn’t specific therapyNeedn’t specific therapy, If the patient has , If the patient has severe symptoms, planted an pacemaker may severe symptoms, planted an pacemaker may be needed.be needed.
Sinus Arrest or Sinus Sinus Arrest or Sinus StandstillStandstill
Sinus arrest or standstill is recognized Sinus arrest or standstill is recognized by a pause in the sinus rhythm. by a pause in the sinus rhythm.
Causes:Causes: myocardial ischemia, hypoxia, myocardial ischemia, hypoxia, hyperkalemia, higher intracranial hyperkalemia, higher intracranial pressure, sinus node degeneration and pressure, sinus node degeneration and some drugs (digitalis, some drugs (digitalis, ß-blocks)ß-blocks)..
Symptoms:Symptoms: dizziness, amaurosis, dizziness, amaurosis, syncopesyncope
TherapyTherapy is same to SSS is same to SSS
Sinoatrial exit block (SAB)Sinoatrial exit block (SAB)
SAB: Sinus pulse was blocked so it SAB: Sinus pulse was blocked so it couldn’t active the atrium.couldn’t active the atrium.
Causes: CAD, Myopathy, Myocarditis, Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al.digitalis toxicity, et al.
Symptoms: dizziness, fatigue, syncopeSymptoms: dizziness, fatigue, syncope
Therapy is same to SSSTherapy is same to SSS
Sinoatrial exit block (SAB)Sinoatrial exit block (SAB)
Divided into three types: Type I, II, IIIDivided into three types: Type I, II, III
Only type II SAB can be recognized by Only type II SAB can be recognized by EKG.EKG.
Sick Sinus Syndrome (SSS)Sick Sinus Syndrome (SSS)SSS: The function of sinus node was SSS: The function of sinus node was degenerated. SSS encompasses both degenerated. SSS encompasses both disordered SA node automaticity and SA disordered SA node automaticity and SA conduction.conduction.
Causes: CAD, SAN degeneration, myopathy, Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, connective tissue disease, metabolic disease, tumor, trauma and congenital disease.tumor, trauma and congenital disease.
With marked sinus bradycardia, sinus arrest, With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythmssinus exit block or junctional escape rhythms
Bradycardia-tachycardia syndromeBradycardia-tachycardia syndrome
Sick Sinus Syndrome (SSS)Sick Sinus Syndrome (SSS)
EKG Recognition:EKG Recognition:1.1. Sinus bradycardia, ≤40 bpm; Sinus bradycardia, ≤40 bpm;
2.2. Sinus arrest > 3sSinus arrest > 3s
3.3. Type II SABType II SAB
4.4. Nonsinus tachyarrhythmia ( SVT, AF or Af).Nonsinus tachyarrhythmia ( SVT, AF or Af).
5.5. SNRT > 1530ms, SNRTc > 525msSNRT > 1530ms, SNRTc > 525ms
6.6. Instinct heart rate < 80bmpInstinct heart rate < 80bmp
Sick Sinus Syndrome (SSS)Sick Sinus Syndrome (SSS)
Therapy:Therapy:1.1. Treat the etiologyTreat the etiology
2.2. Treat with drugs: anti-bradycardia Treat with drugs: anti-bradycardia agents, the effect of drug therapy is agents, the effect of drug therapy is not good.not good.
3.3. Artificial cardiac pacing.Artificial cardiac pacing.
Atrial arrhythmiaAtrial arrhythmia
Premature contractionsPremature contractions
The term “premature contractions” The term “premature contractions” are used to describe non sinus beats. are used to describe non sinus beats.
Common arrhythmiaCommon arrhythmia
The morbidity rate is 3-5%The morbidity rate is 3-5%
Atrial premature contractions Atrial premature contractions (APCs)(APCs)
APCs arising from somewhere in either the left APCs arising from somewhere in either the left or the right atrium.or the right atrium.Causes:Causes: rheumatic heart disease, CAD, rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemiahypertension, hyperthyroidism, hypokalemiaSymptoms:Symptoms: many patients have no symptom, many patients have no symptom, some have palpitation, chest incomfortable.some have palpitation, chest incomfortable.Therapy:Therapy: Needn’t therapy in the patients Needn’t therapy in the patients without heart disease. Can be treated with without heart disease. Can be treated with ß-ß-blocker, propafenone, moricizine or verapamil.blocker, propafenone, moricizine or verapamil.
Atrial tachycardiaAtrial tachycardia
ClassifyClassify by automatic atrial tachycardia by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (IART); chaotic atrial tachycardia (CAT).tachycardia (CAT).
Etiology: atrial enlargement, MI; chronic Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; metabolic disturbance; digitalis toxicity; electrolytic disturbance.electrolytic disturbance.
Atrial tachycardiaAtrial tachycardia
May occur transient; intermittent; or May occur transient; intermittent; or persistent. persistent.
Symptoms: palpitation; chest Symptoms: palpitation; chest uncomfortable, tachycardia may induce uncomfortable, tachycardia may induce myopathy.myopathy.
Auscultation: the first heart sound is Auscultation: the first heart sound is variablevariable
Intra-atrial reentry tachycardia Intra-atrial reentry tachycardia (IART)(IART)
ECG characters:ECG characters:
1.1. Atrial rate is around 130-150bpm;Atrial rate is around 130-150bpm;
2.2. P’ wave is different from sinus P wave;P’ wave is different from sinus P wave;
3.3. P’-R interval ≥ 0.12”P’-R interval ≥ 0.12”
4.4. Often appear type I or type II, 2:1 AV block;Often appear type I or type II, 2:1 AV block;
5.5. EP study: atrial program pacing can EP study: atrial program pacing can induce and terminate tachycardiainduce and terminate tachycardia
Automatic atrial tachycardia Automatic atrial tachycardia (AAT)(AAT)
ECG characters:ECG characters:1.1. Atrial rate is around 100-200bpm;Atrial rate is around 100-200bpm;2.2. Warmup phenomenaWarmup phenomena3.3. P’ wave is different from sinus P wave;P’ wave is different from sinus P wave;4.4. P’-R interval≥ 0.12”P’-R interval≥ 0.12”5.5. Often appear type I or type II, 2:1 AV Often appear type I or type II, 2:1 AV
block;block;6.6. EP study: Atrial program pacing can’t EP study: Atrial program pacing can’t
induce or terminate the tachycardiainduce or terminate the tachycardia
Chaotic atrial tachycardia Chaotic atrial tachycardia (CAT)(CAT)Also termed “Multifocal atrial tachycardia”.Also termed “Multifocal atrial tachycardia”.
Always occurs in COPD or CHF, Always occurs in COPD or CHF, Have a high in-hospital mortality ( 25-56%). Have a high in-hospital mortality ( 25-56%). Death is caused by the severity of the Death is caused by the severity of the underlying disease.underlying disease. ECG characters:ECG characters:
1.1. Atrial rate is around 100-130bpm;Atrial rate is around 100-130bpm;2.2. The morphologies P’ wave are more than 3 The morphologies P’ wave are more than 3
types.types.3.3. P’-P’, P’-R and R-R interval are different.P’-P’, P’-R and R-R interval are different.4.4. Will progress to af in half the casesWill progress to af in half the cases5.5. EP study: Atrial program pacing can’t EP study: Atrial program pacing can’t
induce or terminate the tachycardiainduce or terminate the tachycardia
TherapyTherapy
IRAT:IRAT: Esophageal Pulsation Modulation, Esophageal Pulsation Modulation, RFCA, Ic and IV class anti-tachycardia RFCA, Ic and IV class anti-tachycardia agentsagents
AAT: Digoxin, IV, II, Ia and III class anti-AAT: Digoxin, IV, II, Ia and III class anti-tachycardia agents; RFCAtachycardia agents; RFCA
CAT: treat the underlying disease, CAT: treat the underlying disease, verapamil or amiodarone.verapamil or amiodarone.
Associated with SSS: Implant pace-Associated with SSS: Implant pace-maker. maker.
Atrial flutterAtrial flutter
Etiology:Etiology:1.1. It can occur in patients with normal It can occur in patients with normal
atrial or with abnormal atrial.atrial or with abnormal atrial.2.2. It is seen in rheumatic heart It is seen in rheumatic heart
disease (mitral or tricuspid valve disease (mitral or tricuspid valve disease), CAD, hypertension, disease), CAD, hypertension, hyperthyroidism, congenital heart hyperthyroidism, congenital heart disease, COPD. disease, COPD.
3.3. Related to enlargement of the atriaRelated to enlargement of the atria4.4. Most AF have a reentry loop in Most AF have a reentry loop in
right atrialright atrial
Atrial flutterAtrial flutter
Symptoms:Symptoms: depend on underlying depend on underlying disease, ventricular rate, the patient is disease, ventricular rate, the patient is at rest or is exerting at rest or is exerting
With rapid ventricular rate: palpitation, With rapid ventricular rate: palpitation, dizziness, shortness of breath, dizziness, shortness of breath, weakness, faintness, syncope, may weakness, faintness, syncope, may develop angina and CHF.develop angina and CHF.
Atrial flutterAtrial flutter
Therapy:Therapy:1.1. Treat the underlying diseaseTreat the underlying disease2.2. To restore sinus rhythm: To restore sinus rhythm:
Cardioversion,Cardioversion, Esophageal Pulsation Esophageal Pulsation Modulation, RFCA, Drug (III, Ia, Ic Modulation, RFCA, Drug (III, Ia, Ic class).class).
3.3. Control the ventricular rate: digitalis. Control the ventricular rate: digitalis. CCB, CCB, ß-blockß-block
4.4. Anticoagulation Anticoagulation
Atrial fibrillationAtrial fibrillationSubdivided into three types: paroxysmal, Subdivided into three types: paroxysmal, persistent, permanent.persistent, permanent. Etiology:Etiology:
1.1. Morbidity rate increase in older patientsMorbidity rate increase in older patients2.2. Etiology just like atrial flutterEtiology just like atrial flutter3.3. IdiopathicIdiopathic
Mechanism:Mechanism: 1.1. Multiple wavelet re-entry;Multiple wavelet re-entry;2.2. Rapid firing focus in pulmonary vein, Rapid firing focus in pulmonary vein,
vena cava or coronary sinus.vena cava or coronary sinus.
Atrial fibrillationAtrial fibrillationManifestation:Manifestation:
Affected by underlying diseases, ventricular rate Affected by underlying diseases, ventricular rate and heart function. and heart function.
May develop embolism in left atrial. Have high May develop embolism in left atrial. Have high incidence of stroke.incidence of stroke.
The heart rate, S1 and rhythm is irregularly The heart rate, S1 and rhythm is irregularly irregularirregular
If the heart rhythm is regular, should consider If the heart rhythm is regular, should consider about (1) restore sinus rhythm; (2) AF with about (1) restore sinus rhythm; (2) AF with constant the ratio of AV conduction; (3) constant the ratio of AV conduction; (3) junctional or ventricular tachycardia; (4) slower junctional or ventricular tachycardia; (4) slower ventricular rate may have complete AV block.ventricular rate may have complete AV block.
Atrial fibrillationAtrial fibrillation
Therapy:Therapy:1.1. Treat the underlying diseaseTreat the underlying disease2.2. Restore sinus rhythm: Drug, Restore sinus rhythm: Drug,
Cardioversion, RFCA, Maze surgeryCardioversion, RFCA, Maze surgery3.3. Rate control:Rate control: digitalis. CCB, digitalis. CCB, ß-blockß-block4.4. Antithrombotic therapy: Aspirine, Antithrombotic therapy: Aspirine,
WarfarinWarfarin
Atrioventricular Junctional Atrioventricular Junctional arrhythmiaarrhythmia
Atrioventricular junctional Atrioventricular junctional premature contractionspremature contractions
Etiology and manifestation is like Etiology and manifestation is like APCsAPCs
Therapy the underlying diseaseTherapy the underlying disease
Needn’t anti-arrhythmia therapy.Needn’t anti-arrhythmia therapy.
Nonparoxysmal AV junctional Nonparoxysmal AV junctional tachycardiatachycardia
Mechanism:Mechanism: relate to hyper- relate to hyper-automaticity or trigger activity of AV automaticity or trigger activity of AV junctional tissuejunctional tissue
Etiology:Etiology: digitalis toxicity; inferior MI; digitalis toxicity; inferior MI; myocarditis; acute rheumatic fever and myocarditis; acute rheumatic fever and postoperation of valve diseasepostoperation of valve disease
ECG:ECG: the heart rate ranges 70-150 bpm the heart rate ranges 70-150 bpm or more, regular, normal QRS complex, or more, regular, normal QRS complex, may occur AV dissociation and may occur AV dissociation and wenckebach AV block wenckebach AV block
Nonparoxysmal AV junctional Nonparoxysmal AV junctional tachycardiatachycardia
Therapy:Therapy:
Treat underlying disease; stopping Treat underlying disease; stopping digoxin, administer potassium, digoxin, administer potassium, lidocaine, phenytoin or propranolol.lidocaine, phenytoin or propranolol.
Not for DC shockNot for DC shock
It can disappear spontaneously. If It can disappear spontaneously. If had good tolerance, not require had good tolerance, not require therapy.therapy.
Paroxysmal tachycardiaParoxysmal tachycardia
Most PSVT (paroxysmal supraventricular Most PSVT (paroxysmal supraventricular tachycardia) is due to reentrant mechanism. tachycardia) is due to reentrant mechanism.
The incidence of PSVT is higher in AVNRT The incidence of PSVT is higher in AVNRT (atrioventricular node reentry tachycardia) (atrioventricular node reentry tachycardia) and AVRT (atioventricular reentry and AVRT (atioventricular reentry tachycardia), the most common is AVNRT tachycardia), the most common is AVNRT (90%)(90%)
Occur in any age individuals, usually no Occur in any age individuals, usually no structure heart disease.structure heart disease.
Paroxysmal tachycardiaParoxysmal tachycardiaManifestation:Manifestation: Occur and terminal abruptly.Occur and terminal abruptly.
Palpitation, dizziness, syncope, Palpitation, dizziness, syncope, angina, heart failure and shock.angina, heart failure and shock.The sever degree of the The sever degree of the symptom is related to symptom is related to ventricular rate, persistent ventricular rate, persistent duration and underlying duration and underlying diseasedisease
Paroxysmal tachycardiaParoxysmal tachycardia
ECG characteristic of AVNRTECG characteristic of AVNRT
1.1. Heart rate is 150-250 bpm, regular Heart rate is 150-250 bpm, regular
2.2. QRS complex is often normal, wide QRS complex is often normal, wide QRS complex is with aberrant QRS complex is with aberrant conductionconduction
3.3. Negative P wave in II III aVF, buried Negative P wave in II III aVF, buried into or following by the QRS complex. into or following by the QRS complex.
4.4. AVN jump phenomenaAVN jump phenomena
Paroxysmal tachycardiaParoxysmal tachycardia
ECG characteristic of AVRTECG characteristic of AVRT
1.1. Heart rate is 150-250 bpm, regular Heart rate is 150-250 bpm, regular
2.2. In orthodromic AVRT, the QRS complex In orthodromic AVRT, the QRS complex is often normal, wide QRS complex is is often normal, wide QRS complex is with antidromic AVRTwith antidromic AVRT
3.3. Retrograde P’ wave, R-P’>110ms. Retrograde P’ wave, R-P’>110ms.
Paroxysmal tachycardiaParoxysmal tachycardia
Therapy:Therapy: AVNRT & orthodromic AVRTAVNRT & orthodromic AVRT
1.1. Increase vagal tone: carotid sinus Increase vagal tone: carotid sinus massage, Valsalva maneuver.if no massage, Valsalva maneuver.if no successful, successful,
2.2. Drug: verapamil, adrenosine, propafenoneDrug: verapamil, adrenosine, propafenone3.3. DC shockDC shock
Antidromic AVRT:Antidromic AVRT:1.1. Should not use verapamil, digitalis, and Should not use verapamil, digitalis, and
stimulate the vagal nerve.stimulate the vagal nerve.2.2. Drug: propafenone, sotalol, amiodarone Drug: propafenone, sotalol, amiodarone
RFCARFCA
Pre-excitation syndromePre-excitation syndrome(W-P-W syndrome)(W-P-W syndrome)
There are several type of accessory There are several type of accessory pathwaypathway
1.1. Kent: adjacent atrial and ventricular Kent: adjacent atrial and ventricular
2.2. James: adjacent atrial and his James: adjacent atrial and his bundlebundle
3.3. Mahaim: adjacent lower part of the Mahaim: adjacent lower part of the AVN and ventricularAVN and ventricular
Usually no structure heart disease, Usually no structure heart disease, occur in any age individualoccur in any age individual
WPW syndromeWPW syndrome
Manifestation:Manifestation:
Palpitation, syncope, dizziness Palpitation, syncope, dizziness
Arrhythmia: 80% tachycardia is Arrhythmia: 80% tachycardia is AVRT, 15-30% is AFi, 5% is AF, AVRT, 15-30% is AFi, 5% is AF,
May induce ventricular fibrillationMay induce ventricular fibrillation
WPW syndromeWPW syndromeTherapy:Therapy:
1.1. Pharmacologic therapy: orthodrome Pharmacologic therapy: orthodrome AVRT or associated AF, AFi, may use AVRT or associated AF, AFi, may use Ic and III class agents. Ic and III class agents.
2.2. Antidromic AVRT can’t use digoxin Antidromic AVRT can’t use digoxin and verapamil.and verapamil.
3.3. DC shock: WPW with SVT, AF or Afi DC shock: WPW with SVT, AF or Afi produce agina, syncope and produce agina, syncope and hypotensionhypotension
4.4. RFCARFCA
Ventricular arrhythmiaVentricular arrhythmia
Ventricular Premature Ventricular Premature Contractions (VPCs)Contractions (VPCs)
Etiology:Etiology:
1.1. Occur in normal personOccur in normal person
2.2. Myocarditis, CAD, valve heart disease, Myocarditis, CAD, valve heart disease, hyperthyroidism, Drug toxicity hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety (digoxin, quinidine and anti-anxiety drug)drug)
3.3. electrolyte disturbance, anxiety, electrolyte disturbance, anxiety, drinking,drinking, coffeecoffee
VPCsVPCs
Manifestation: Manifestation:
1.1. palpitationpalpitation
2.2. dizzinessdizziness
3.3. syncope syncope
4.4. loss of the second heart soundloss of the second heart sound
PVCsPVCsTherapy:Therapy: treat underlying disease, treat underlying disease, antiarrhythmiaantiarrhythmia
No structure heart disease:No structure heart disease:
1.1. Asymptom: no therapy Asymptom: no therapy
2.2. Symptom caused by PVCs: antianxiety agents, Symptom caused by PVCs: antianxiety agents, ßß-blocker and mexiletine to relief the symptom.-blocker and mexiletine to relief the symptom.
With structure heart disease (CAD, HBP):With structure heart disease (CAD, HBP):
1.1. Treat the underlying diseasTreat the underlying diseas
2.2. ßß-blocker, amiodarone-blocker, amiodarone
3.3. Class I especially class Ic agents should be Class I especially class Ic agents should be avoided because of proarrhytmia and lack of avoided because of proarrhytmia and lack of benefit of prophylaxisbenefit of prophylaxis
Ventricular tachycardiaVentricular tachycardia
Etiology: often in organic heart disease Etiology: often in organic heart disease
CAD, MI, DCM, HCM, HF, CAD, MI, DCM, HCM, HF,
long QT syndrome long QT syndrome
Brugada syndromeBrugada syndrome
Sustained VT (>30s), Nonsustained VTSustained VT (>30s), Nonsustained VT
Monomorphic VT, Polymorphic VTMonomorphic VT, Polymorphic VT
Ventricular tachycardiaVentricular tachycardiaTorsades de points (Tdp):Torsades de points (Tdp): A special type of A special type of polymorphic VT, polymorphic VT,
Etiology:Etiology:
1.1. congenital (Long QT), congenital (Long QT),
2.2. electrolyte disturbance, electrolyte disturbance,
3.3. antiarrhythmia drug proarrhythmia (IA or antiarrhythmia drug proarrhythmia (IA or IC), IC),
4.4. antianxiety drug, antianxiety drug,
5.5. brain disease, brain disease,
6.6. bradycardiabradycardia
Ventricular tachycardiaVentricular tachycardia
Accelerated idioventricular rhythm:Accelerated idioventricular rhythm:
1.1. Related to increase automatic toneRelated to increase automatic tone
2.2. EtiologyEtiology: Often occur in organic heart : Often occur in organic heart disease, especially AMI reperfusion disease, especially AMI reperfusion periods, heart operation, myocarditis, periods, heart operation, myocarditis, digitalis toxicitydigitalis toxicity
VTVT
Manifestation: Manifestation:
1.1. Nonsustained VT with no symptom Nonsustained VT with no symptom
2.2. Sustained VT : with symptom and Sustained VT : with symptom and unstable hemodynamic, patient unstable hemodynamic, patient may feel palpitation, short of may feel palpitation, short of breathness, presyncope, syncope, breathness, presyncope, syncope, angina, hypotension and shock.angina, hypotension and shock.
VTVT
ECG characteristics:ECG characteristics:
1.1. Monomorphic VT: 100-250 bpm, occur and Monomorphic VT: 100-250 bpm, occur and terminate abruptly,regular terminate abruptly,regular
2.2. Accelerated idioventricular rhythm: a runs of 3-Accelerated idioventricular rhythm: a runs of 3-10 ventricular beats, rate of 60-110 bpm, 10 ventricular beats, rate of 60-110 bpm, tachycardia is a capable of warm up and close tachycardia is a capable of warm up and close down, often seen AV dissociation, fusion or down, often seen AV dissociation, fusion or capture beats capture beats
3.3. Tdp: rotation of the QRS axis around the Tdp: rotation of the QRS axis around the baseline, the rate from 160-280 bpm, QT interval baseline, the rate from 160-280 bpm, QT interval prolonged > 0.5s, marked U waveprolonged > 0.5s, marked U wave
Treatment of VTTreatment of VT
1.1. Treat underlying diseaseTreat underlying disease
2.2. Cardioversion: Hemodynamic Cardioversion: Hemodynamic unstable VT (hypotension, shock, unstable VT (hypotension, shock, angina, CHF) or hemodynamic angina, CHF) or hemodynamic stable but drug was no effectstable but drug was no effect
3.3. Pharmacological therapy: Pharmacological therapy: ß-ß-blockers, blockers, lidocain or amiodaronelidocain or amiodarone
4.4. RFCA, ICD or surgical therapyRFCA, ICD or surgical therapy
Therapy of Special type VTTherapy of Special type VT
Accelerated idioventricular rhythm:Accelerated idioventricular rhythm:
usually no symptom, needn’t therapy. usually no symptom, needn’t therapy.
Atropine increased sinus rhythmAtropine increased sinus rhythm
Tdp:Tdp:
1.1. Treat underlying disease, Treat underlying disease,
2.2. Magnesium iv, atropine or Magnesium iv, atropine or isoprenaline, isoprenaline, ßß-block or pacemaker for -block or pacemaker for long QT patientlong QT patient
3.3. temporary pacemakertemporary pacemaker
Ventricular flutter and fibrillationVentricular flutter and fibrillation
Often occur in severe organic heart Often occur in severe organic heart disease: AMI, ischemia heart diseasedisease: AMI, ischemia heart disease
Proarrhythmia (especially produce long Proarrhythmia (especially produce long QT and Tdp), electrolyte disturbanceQT and Tdp), electrolyte disturbance
Anaesthesia, lightning strike, electric Anaesthesia, lightning strike, electric shock, heart operationshock, heart operation
It’s a fatal arrhythmiaIt’s a fatal arrhythmia
Ventricular flutter and fibrillationVentricular flutter and fibrillation
Manifestation:Manifestation:
Unconsciousness, twitch, no blood Unconsciousness, twitch, no blood pressure and pulse, going to diepressure and pulse, going to die
Therapy:Therapy:
1.1. Cardio-Pulmonary ResuscitateCardio-Pulmonary Resuscitate (CPR)(CPR)
2.2. ICDICD
Cardiac conduction blockCardiac conduction block
Block position:Block position:
Sinoatrial; intra-atrial; Sinoatrial; intra-atrial; atrioventricular; intra-ventricularatrioventricular; intra-ventricular
Block degreeBlock degree
1.1. Type I: prolong the conductive timeType I: prolong the conductive time
2.2. Type II: partial blockType II: partial block
3.3. Type III: complete blockType III: complete block
Atrioventricular BlockAtrioventricular Block
AV block is a delay or failure in AV block is a delay or failure in transmission of the cardiac impulse transmission of the cardiac impulse from atrium to ventricle.from atrium to ventricle.
Etiology:Etiology:
Atherosclerotic heart disease; Atherosclerotic heart disease; myocarditis; rheumatic fever; myocarditis; rheumatic fever; cardiomyopathy; drug toxicity; cardiomyopathy; drug toxicity; electrolyte disturbance, collagen electrolyte disturbance, collagen disease, lev’s disease.disease, lev’s disease.
AV BlockAV Block
AV block is divided into three AV block is divided into three categories:categories:
1.1. First-degree AV blockFirst-degree AV block
2.2. Second-degree AV block: further Second-degree AV block: further subdivided into type I and type IIsubdivided into type I and type II
3.3. Third-degree AV block: complete Third-degree AV block: complete blockblock
AV BlockAV Block
Manifestations:Manifestations:
First-degree AV block: almost no symptoms;First-degree AV block: almost no symptoms;
Second degree AV block: palpitation, fatigueSecond degree AV block: palpitation, fatigue
Third degree AV block: Dizziness, agina, heart Third degree AV block: Dizziness, agina, heart failure, lightheadedness, and syncope may failure, lightheadedness, and syncope may cause by slow heart rate, Adams-Stokes cause by slow heart rate, Adams-Stokes Syndrome may occurs in sever case.Syndrome may occurs in sever case.
First heart sound varies in intensity, will First heart sound varies in intensity, will appear booming first soundappear booming first sound
AV BlockAV Block
Treatment:Treatment:
1.1. I or II degree AV block needn’t I or II degree AV block needn’t antibradycardia agent therapyantibradycardia agent therapy
2.2. II degree II type and III degree AV II degree II type and III degree AV block need antibradycardia agent block need antibradycardia agent therapytherapy
3.3. Implant Pace MakerImplant Pace Maker
Intraventricular BlockIntraventricular Block
Intraventricular conduction system:Intraventricular conduction system:
1.1. Right bundle branchRight bundle branch
2.2. Left bundle branchLeft bundle branch
3.3. Left anterior fascicularLeft anterior fascicular
4.4. Left posterior fascicularLeft posterior fascicular
Intraventricular BlockIntraventricular Block
Etiology:Etiology:Myocarditis, valve disease, Myocarditis, valve disease, cardiomyopathy, CAD, hypertension, cardiomyopathy, CAD, hypertension, pulmonary heart disease, drug toxicity, pulmonary heart disease, drug toxicity, Lenegre disease, Lev’s disease et al.Lenegre disease, Lev’s disease et al.Manifestation:Manifestation:Single fascicular or bifascicular block is Single fascicular or bifascicular block is asymptom; tri-fascicular block may asymptom; tri-fascicular block may have dizziness; palpitation, syncope have dizziness; palpitation, syncope and Adams-stokes syndromeand Adams-stokes syndrome
Intraventricular BlockIntraventricular Block
Therapy:Therapy:
1.1. Treat underlying diseaseTreat underlying disease
2.2. If the patient is asymptom; no treat,If the patient is asymptom; no treat,
3.3. bifascicular block and incomplete bifascicular block and incomplete trifascicular block may progress to trifascicular block may progress to complete block, may need implant complete block, may need implant pace maker if the patient with syncopepace maker if the patient with syncope
Cardiac Arrhythmias: An UpdateCardiac Arrhythmias: An Update
Dr N.M.GandhiDr N.M.GandhiConsultant CardiologistConsultant Cardiologist
Spire Gatwick Park Hospital, HorleySpire Gatwick Park Hospital, HorleyEast Surrey Hospital, RedhillEast Surrey Hospital, Redhill
Royal Sussex County Hospital, BrightonRoyal Sussex County Hospital, Brighton
ObjectivesObjectives
Identify common arrhythmias encountered by Identify common arrhythmias encountered by the family physicianthe family physician
Discuss initial Mg options Discuss initial Mg options
AF and Ventricular arrhythmias case studies AF and Ventricular arrhythmias case studies
Which patients needs to be referred? ECG Which patients needs to be referred? ECG examplesexamples
THE CONDUCTION THE CONDUCTION SYSTEMSYSTEM
Atrial DepolarizationAtrial Depolarization
Ventricular DepolarizationVentricular Depolarization
CARDIAC ARRHYTHMIASCARDIAC ARRHYTHMIAS
Disturbances of either :Disturbances of either :
Impulse generationImpulse generation
Impulse propagationImpulse propagation
ARRHYTHMIAS
ELECTROPHYSIOLOGIC PRINCIPLES
BRADYARRHYTHMIAS
• SINUS NODE DYSFUNCTION• AV CONDUCTION DISTURBANCES
TACHYARRHYTMIAS
•ATRIAL TACHYCARDIAS•VENTRICULAR TACHYCARDIA
BradyarrhythmiasBradyarrhythmiasImpulse formation:Impulse formation:– Decreased automaticity: Sinus bradycardiaDecreased automaticity: Sinus bradycardia
Impulse conduction:Impulse conduction:– Conduction blocks: 1º, 2º, 3º AV blocksConduction blocks: 1º, 2º, 3º AV blocks
TachyarrythmiasTachyarrythmiasImpulse formationImpulse formation– Enhanced automaticity:Enhanced automaticity:
Sinus node: sinus tachycardiaSinus node: sinus tachycardiaEctopic focus: Ectopic atrial tachycardiaEctopic focus: Ectopic atrial tachycardia
– Triggered activityTriggered activityEarly afterdepolarization: torsades de pointesEarly afterdepolarization: torsades de pointesDigitalis-induced SVTDigitalis-induced SVT
Impulse conductionImpulse conduction– Reentry: Paroxysmal SVT, atrial flutter and fibrilation, Reentry: Paroxysmal SVT, atrial flutter and fibrilation,
ventricular tachycardia and fibrillation.ventricular tachycardia and fibrillation.
Normal Sinus RhythmNormal Sinus Rhythm
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
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PACPAC
Benign, common cause of perceived Benign, common cause of perceived irregular rhythmirregular rhythmCan cause sxs: “skipping” beats, Can cause sxs: “skipping” beats, palpitationspalpitationsNo treatment, reassuranceNo treatment, reassuranceWith sxs, may advise to stop smoking, With sxs, may advise to stop smoking, decrease caffeine and ETOHdecrease caffeine and ETOHCan use beta-blockers to reduce Can use beta-blockers to reduce frequencyfrequency
PVCPVC
Extremely common throughout the population, both with Extremely common throughout the population, both with and without heart diseaseand without heart diseaseUsually asymptomatic, except rarely dizziness or fatigue Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV in patients that have frequent PVCs and significant LV dysfunctiondysfunction
PVCPVC
ReassuranceReassurance
Optimize cardiac and pulmonary disease Optimize cardiac and pulmonary disease managementmanagement
Beta-blockerBeta-blocker
Ablation in a small number of casesAblation in a small number of cases
BradyarrhythmiasBradyarrhythmiasImpulse formation:Impulse formation:– Decreased automaticity: Sinus bradycardiaDecreased automaticity: Sinus bradycardia
Impulse conduction:Impulse conduction:– Conduction blocks: 1º, 2º, 3º AV blocksConduction blocks: 1º, 2º, 3º AV blocks
Sinus BradycardiaSinus Bradycardia
HR< 60 bpm; every QRS narrow, preceded by p waveHR< 60 bpm; every QRS narrow, preceded by p wave
Can be normal in well-conditioned athletesCan be normal in well-conditioned athletes
HR can be 30 bpm in adults during sleep, with up to 2 HR can be 30 bpm in adults during sleep, with up to 2 sec pausessec pauses
Sinus arrhythmiaSinus arrhythmia
Usually respiratory--Increase in heart rate during Usually respiratory--Increase in heart rate during inspirationinspirationExaggerated in children, young adults and Exaggerated in children, young adults and athletes—decreases with ageathletes—decreases with ageUsually asymptomatic, no treatment or referralUsually asymptomatic, no treatment or referralCan be non-respiratory, often in normal or Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicitydiseased heart, seen in digitalis toxicityReferral may be necessary if not clearly Referral may be necessary if not clearly respiratory, history of heart diseaserespiratory, history of heart disease
Sick Sinus SyndromeSick 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.
11stst Degree AV Block Degree AV Block
PR interval >200msPR interval >200ms
If accompanied by wide QRS, refer to cardiology, high If accompanied by wide QRS, refer to cardiology, high risk of progression to 2risk of progression to 2ndnd and 3 and 3rdrd deg block deg block
Otherwise, benign if asymptomaticOtherwise, benign if asymptomatic
22ndnd Degree AV Block Mobitz type I Degree AV Block Mobitz type I (Wenckebach)(Wenckebach)
Progressive PR longation, with eventual non-Progressive PR longation, with eventual non-conduction of a p waveconduction of a p waveMay be in 2:1 or 3:1 May be in 2:1 or 3:1
22ndnd degree block Type II (Mobitz 2) degree block Type II (Mobitz 2)
Normal PR intervals with sudden failure of a p wave to conductNormal PR intervals with sudden failure of a p wave to conductUsually below AV node and accompanied by BBB or fascicular Usually below AV node and accompanied by BBB or fascicular blockblockOften causes pre/syncope; exercise worsens sxsOften causes pre/syncope; exercise worsens sxsGenerally need pacing, possibly urgently if symptomaticGenerally need pacing, possibly urgently if symptomatic
33rdrd Degree AV Block Degree AV Block
Complete AV disassociation, HR is a ventricular rateComplete AV disassociation, HR is a ventricular rate
Will often cause dizziness, syncope, angina, heart failureWill often cause dizziness, syncope, angina, heart failure
Can degenerate to Vtach and VfibCan degenerate to Vtach and Vfib
Will need pacing, urgent referralWill need pacing, urgent referral
TachyarrythmiasTachyarrythmiasImpulse formationImpulse formation– Enhanced automaticity:Enhanced automaticity:
Sinus node: sinus tachycardiaSinus node: sinus tachycardiaEctopic focus: Ectopic atrial tachycardiaEctopic focus: Ectopic atrial tachycardia
– Triggered activityTriggered activityEarly afterdepolarization: torsades de pointesEarly afterdepolarization: torsades de pointesDigitalis-induced SVTDigitalis-induced SVT
Impulse conductionImpulse conduction– Reentry: Paroxysmal SVT, atrial flutter and fibrilation, Reentry: Paroxysmal SVT, atrial flutter and fibrilation,
ventricular tachycardia and fibrillation.ventricular tachycardia and fibrillation.
SUPRAVENTRICULAR T. SUPRAVENTRICULAR T.
Sinus TachycardiaSinus Tachycardia
Atrial flutterAtrial flutter
Atrial fibrilationAtrial fibrilation
Paroxysmal SupraventricularParoxysmal Supraventricular
Multifocal Atrial T.Multifocal Atrial T.Preexcitation Syndrome Preexcitation Syndrome (Wolff-Parkinson-white Sy.)(Wolff-Parkinson-white Sy.)
Sinus tachycardiaSinus tachycardia
HR > 100 bpm, regularHR > 100 bpm, regular
Often difficult to distinguish p and t wavesOften difficult to distinguish p and t waves
Paroxysmal Supraventricular T.Paroxysmal Supraventricular T.
Sudden onset and terminationSudden onset and termination
Atrial rates of 140 to 250 /minAtrial rates of 140 to 250 /min
Normal QRS complexes Normal QRS complexes
The mechanism is most often reentry.The mechanism is most often reentry.
Paroxysmal Supraventricular Paroxysmal Supraventricular TachycardiaTachycardia
Refers to supraventricular tachycardia other Refers to supraventricular tachycardia other than afib, aflutter and MATthan afib, aflutter and MAT
Usually due to reentry—AVNRT or AVRTUsually due to reentry—AVNRT or AVRT
PSVTPSVT
CSM or adenosine commonly terminate CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRTthe arrhythmia, esp, AVRT or AVNRT
Can also use CCB or beta blockers to Can also use CCB or beta blockers to terminate, if availableterminate, if available
Counsel to avoid triggers, caffeine, Etoh, Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stresspseudoephedrine, stress
Multifocal Atrial T.Multifocal Atrial T.Is due to enchanced automaticity within Is due to enchanced automaticity within the atria, resulting in abnormal discharges the atria, resulting in abnormal discharges from several ectopic focifrom several ectopic fociMost often occurs in the setting of severe Most often occurs in the setting of severe pulmonary disease and hypoxemia.pulmonary disease and hypoxemia.EKG: irregular rhythm with multiple (at EKG: irregular rhythm with multiple (at leats 3) P waves morphologiesleats 3) P waves morphologies
Atrial flutterAtrial flutter
Is caracterized by rapid coarse “sawtooth” appearing atrial Is caracterized by rapid coarse “sawtooth” appearing atrial activity, at rate of 250 to 350 x min.activity, at rate of 250 to 350 x min.
– Many of these fast impulses reach the AV node during Many of these fast impulses reach the AV node during its refractory period, so that the ventricular rate is its refractory period, so that the ventricular rate is generally lower.generally lower.
Frequently it degenerates into atrial fibrilationFrequently it degenerates into atrial fibrilation
– The most expiditious therapy is electrical cardioversion, The most expiditious therapy is electrical cardioversion, which is undertaken directly for highly symptomatic which is undertaken directly for highly symptomatic patients. (to revert chronic refractory atrial flutter that patients. (to revert chronic refractory atrial flutter that has not responded to other approacheshas not responded to other approaches))
Preexcitation SyndromePreexcitation SyndromeWolff-Parkinson-White SyndromeWolff-Parkinson-White Syndrome
EKG: Although different types of bypass EKG: Although different types of bypass tracts have been identified, the bundle of tracts have been identified, the bundle of Kent, is the most common and can usually Kent, is the most common and can usually conduct in both the anterograde and conduct in both the anterograde and retrograde directions.retrograde directions.
Atrial FibrillationAtrial Fibrillation
Irregular rhythm Irregular rhythm Absence of definite p wavesAbsence of definite p wavesNarrow QRSNarrow QRSCan be accompanied by rapid ventricular responseCan be accompanied by rapid ventricular response
Atrial fibrillation--managementAtrial fibrillation--management
Rhythm vs Rate control—if onset is within last Rhythm vs Rate control—if onset is within last 24-48 hours, may be able to arrange 24-48 hours, may be able to arrange cardioversion—use heparin around procedurecardioversion—use heparin around procedure
Need TEE if valvular disease (high risk of Need TEE if valvular disease (high risk of thrombus)thrombus)
If unable to If unable to definitely definitely conclude onset in last 24-conclude onset in last 24-48 hours: need 4-6 weeks of anticoagulation 48 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 prior to cardioversion, and warfarin for 4-12 weeks afterweeks after
Atrial Fibrillation: Clinical ProblemsAtrial Fibrillation: Clinical Problems
Embolism and stroke (presumably due to LA clot)Embolism and stroke (presumably due to LA clot)
Acute hospitalization with onset of symptomsAcute hospitalization with onset of symptoms
Anticoagulation, especially in older patients (> 75 yr.)Anticoagulation, especially in older patients (> 75 yr.)
Congestive heart failureCongestive heart failure
– Loss of AV synchronyLoss of AV synchrony
– Loss of atrial “kick”Loss of atrial “kick”
– Rate-related cardiomyopathy due to rapid ventricular Rate-related cardiomyopathy due to rapid ventricular responseresponse
Rate-related atrial myopathy and dilatationRate-related atrial myopathy and dilatation
Chronic symptoms and reduced sense of well-beingChronic symptoms and reduced sense of well-being
AF: Medical ManagementAF: Medical Management
Treatment of underlying causeTreatment of underlying cause
Ventricular rate controlVentricular rate control
AnticoagulationAnticoagulation
Antiarrhythmics with a view to restore sinus Antiarrhythmics with a view to restore sinus rhythmrhythm
Control of Ventricular Rate in Control of Ventricular Rate in Atrial FibrillationAtrial Fibrillation
BetablockersBetablockers
Calcium channel blockersCalcium channel blockers
Verapamil, diltiazemVerapamil, diltiazem
Digoxin Digoxin
AmiodaroneAmiodarone
AnticoagulationAnticoagulation
AnticoagulationAnticoagulation
Assessment of bleeding risk should be part of the clinical Assessment of bleeding risk should be part of the clinical assessment of AF patients prior to starting anticoagulationassessment of AF patients prior to starting anticoagulation
Antithrombotic benefits and potential bleeding risks of Antithrombotic benefits and potential bleeding risks of long-term coagulation should be explained and discussed long-term coagulation should be explained and discussed with the patientwith the patient
Aim for a target INR of between 2.0 and 3.0Aim for a target INR of between 2.0 and 3.0
NICE 2006NICE 2006
CHADS 2 scoringCHADS 2 scoring
Any patients with AF with a score of =/>2 Any patients with AF with a score of =/>2 would benefit from being on Warfarinwould benefit from being on Warfarin
CCF CCF
HypertensionHypertension
Age > 75Age > 75
DiabetesDiabetes
Stroke/TIAStroke/TIA
1 point1 point
1 point1 point
1point1point
1 point1 point
2 points2 points
CardioversionCardioversion
Cardioversion Cardioversion
Cardioversion results in SR in at least 90% Cardioversion results in SR in at least 90% of casesof cases
SR is only maintained in 30-50% at one SR is only maintained in 30-50% at one yearyear
Class 1a, 1c and III agents increase Class 1a, 1c and III agents increase likelihood of maintained SR from 30-50% to likelihood of maintained SR from 30-50% to 50-70% at one year50-70% at one year
Follow-up Follow-up
Follow-up after cardioversion should take place Follow-up after cardioversion should take place at 1 month, and the frequency of subsequent at 1 month, and the frequency of subsequent reviews should be tailored to the patientreviews should be tailored to the patient
Reassess the need for anticoagulation at each Reassess the need for anticoagulation at each reviewreview
Catheter Ablation for AFCatheter Ablation for AF
AF AblationAF Ablation
Success rates – approx 70% but may require repeat Success rates – approx 70% but may require repeat procedureprocedure– Often increase in symptoms for first 3-6 months after Often increase in symptoms for first 3-6 months after
procedure does not indicate failureprocedure does not indicate failure
Risks Risks
– – damage to existing conduction mandating pacingdamage to existing conduction mandating pacing– Cardiac perforation/tamponadeCardiac perforation/tamponade– BleedingBleeding– Stroke/thromboembolismStroke/thromboembolism– DeathDeath
Catheter Ablation: IndicationsCatheter Ablation: Indications
Symptomatic patientsSymptomatic patients
Refractory to AntiarrhythmicsRefractory to Antiarrhythmics
Medical therapy contraindicated due to co-morbidities Medical therapy contraindicated due to co-morbidities or intoleranceor intolerance
NICE 2006NICE 2006
Which AF patients need Which AF patients need Specialist Referral?Specialist Referral?
Patients with:Patients with:
- WPW syndrome- WPW syndrome
- Uncontrolled ventricular rate (> 200/min)- Uncontrolled ventricular rate (> 200/min)
- Tachy-brady syndrome- Tachy-brady syndrome
- For rhythm control strategy- For rhythm control strategy
- CCF- CCF
- Intolerant to Drugs- Intolerant to Drugs
- Invasive options - Invasive options
VENTRICULAR VENTRICULAR ARRHYTHMIASARRHYTHMIAS
Ventricular tachycardiaVentricular tachycardia
Torsades De PointesTorsades De Pointes
Ventricular fibrillationVentricular fibrillation
Ventricular tachycardiaVentricular tachycardiaIs divided in 2 categories:Is divided in 2 categories:– If it persist for more than 30 seconds If it persist for more than 30 seconds
“sustained VT”“sustained VT”– Less than 30 seconds: “nonsustained VT”Less than 30 seconds: “nonsustained VT”
Symptoms vary depending on the Symptoms vary depending on the duration.duration.– Major manifestations are hypotension and Major manifestations are hypotension and
loss of consciousness.loss of consciousness.
Non-sustained ventricular tachycardiaNon-sustained ventricular tachycardia
Need to exclude heart disease with Echo and Need to exclude heart disease with Echo and stress testingstress testing
May need anti-arrhythmia treatment if sxsMay need anti-arrhythmia treatment if sxs
In presence of heart disease, increased risk of In presence of heart disease, increased risk of sudden deathsudden death
Need referral for EPS and/or prolonged Holter Need referral for EPS and/or prolonged Holter monitoringmonitoring
ICD may be life savingICD may be life saving
Torsades De PointesTorsades De PointesVarying amplitudes of the QRS.Varying amplitudes of the QRS.
It can be produced by afterdepolarizations It can be produced by afterdepolarizations (triggered activity).(triggered activity).
Particularly in prolonged QT interval.Particularly in prolonged QT interval.
Occur with some drugs (quinidine), Occur with some drugs (quinidine), electrolite disturbances, and congenital electrolite disturbances, and congenital prolongation of the QT interval.prolongation of the QT interval.
Specialist ReferralSpecialist Referral
ECG Examples ECG Examples
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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 Atrial fibrillation –– ECG ECG
1 sec
Rhythm control approachesRhythm control approaches
Electrical cardioversion
Pharmacological agents
Non-pharmacological approaches
Electrical cardioversionElectrical cardioversion
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)
Heart rhythmin atrial fibrillation
Cardioversionshock
Normal heartrhythm
ECGMetalpaddle
Electrical cardioversionElectrical cardioversion
Specialised equipment and Specialised equipment and expertise requiredexpertise required
Unpleasant experience for patientsUnpleasant experience for patients
Good cardioversion rates but risk of Good cardioversion rates but risk of immediate or long-term recurrenceimmediate or long-term recurrence
Pharmacological therapy required to Pharmacological therapy required to prevent recurrences of AFprevent recurrences of AF
Fuster V et al. Eur Heart J 2006;27:1979–2030 www.medicinenet.com
Heart disease?
YesNo (or minimal)
FlecainidePropafenoneSotalol
Hypertension
AmiodaroneDofetilide
LVH greater thanor equal to 1.4 cm
Yes No
FlecainidePropafenoneAmiodarone
DisopyramideProcainamideQuinidine
AmiodaroneDofetilideSotalol
DisopyramideProcainamideQuinidine
Consider non-pharmacologicaloptions
AmiodaroneDofetilide
Maintenance Maintenance therapytherapy
DisopyramideProcainamideQuinidine
AmiodaroneDofetilide
Fuster V et al. Eur Heart J 2006;27:1979–2030
HF CAD
Sotalol
Maze procedure
Intraoperative ablation Elective percutaneous
Ablation and surgical proceduresAblation and surgical procedures
Open-heart surgery for another indicationConcomitant treatmentAblation – radiofrequency, laser, cryotherapyLong-term efficacy 60–70%
Catheter ablation
Paroxysmal AF
Various technologies
Promising technique under development
Persistent/permanent AFOpen-heart surgeryPrimary treatment of AFSelected, highly symptomatic patientsLong-term curative efficacy >90%
Permanent pacemaker therapyPermanent pacemaker therapyAF is not an accepted AF is not an accepted indication unless bradycardia indication unless bradycardia is presentis present
Moderately effective in some Moderately effective in some patientspatients
Highly effective in some Highly effective in some patients with strictly vagal AFpatients with strictly vagal AF
Specific preventive algorithms Specific preventive algorithms under developmentunder development
Ventricular rate controlVentricular rate control Pharmacological agents
Surgical procedures with device implantation
Verapamil, diltiazem
Rate control - calcium channel Rate control - calcium channel blockersblockers
Reduce contractions by blocking the entry of Reduce contractions by blocking the entry of calcium into heart cellscalcium into heart cells
Preferred in patients with heart or lung diseasePreferred in patients with heart or lung disease
Verapamil most commonly prescribedVerapamil most commonly prescribed
Can cause prolonged hypotensionCan cause prolonged hypotension
Rate control - Rate control - -blockers:-blockers:E.g. propranolol, atenololE.g. propranolol, atenolol
Decrease sensitivity to adrenalineDecrease sensitivity to adrenaline
Preferred for young, active patientsPreferred for young, active patients
Not suitable for patients with asthmaNot suitable for patients with asthma
Can cause hypotension and bradycardiaCan cause hypotension and bradycardia
Rate control - digoxinRate control - digoxinMost widely prescribed for rate control Most widely prescribed for rate control
Promotes AF by shortening atrial refractory period Promotes AF by shortening atrial refractory period
Slow onset of effectSlow onset of effect
Little effect on ventricular rate in active patientsLittle effect on ventricular rate in active patients
Sometimes used for conversion or prevention of Sometimes used for conversion or prevention of recurrence of AF – lack of evidence to support recurrence of AF – lack of evidence to support this approachthis approach
Ventricular rate control – ablation and device Ventricular rate control – ablation and device implantationimplantation
Transvenous His ablationTransvenous His ablation
Persistent/permanent AFPersistent/permanent AF
Patients with insufficient rate Patients with insufficient rate control control
Permanent pacemaker neededPermanent pacemaker needed
Anticoagulation therapy needed Anticoagulation therapy needed
Implant devices Implant devices –– pacemaker 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 Implant devices –– pacemaker pacemakerBattery-poweredgenerator
Pacer wire
Pacemaker
Battery-powered generator and pacer wires
Pacing algorithms detect APBs and begin pacing after a premature beat
Implant devices Implant devices –– implantable implantable defibrillatorsdefibrillators
Electrode charge
Implanted CardioverterDefibrillator
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 Percutaneous treatments –– transvenous His ablationtransvenous His ablation
Right Atrium
Left Atrium
PulmonaryVeins
Catheter withelectrode
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
Catheter with electrode is guided to the pulmonary vein ostia in the left atrium
Electrode burns off (or “isolates”) pulmonary vein
Percutaneous treatments – percutaneous elective catheter ablationPercutaneous treatments – percutaneous elective catheter ablation
Right Atrium
Left Atrium
PulmonaryVeins
Catheter withelectrode
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
Target is pulmonary vein
Surgical techniques Surgical techniques –– isolation isolation of pulmonary veinsof pulmonary veins
Both ablation and surgery of the pulmonary veins are newly introduced, specialised techniques
Currently appropriate for selected patients only
Surgical techniques Surgical techniques –– maze maze procedureprocedure
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
Incisions
Cardiac Arrhythmias Cardiac Arrhythmias IIII: Tachyarrhythmias: Tachyarrhythmias
Michael H. Lehmann, M.D.Michael H. Lehmann, M.D.
Clinical Professor of Internal MedicineClinical Professor of Internal Medicine
Director, Electrocardiography LaboratoryDirector, Electrocardiography Laboratory
Supraventricular TachycardiasSupraventricular Tachycardias
((Supraventricular - Supraventricular - a rhythm process a rhythm process in which the ventricles are activated in which the ventricles are activated from the atria or AV node/His bundle from the atria or AV node/His bundle region)region)
Supraventricular Tachycardia (SVT) Terminology
• QRS typically narrow (in absence of bundle branch block); thus, also termed narrow QRS tachycardia
• 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 Tachycardias(typically incorporate AV nodal tissue)
UnidirectionalBlock
Recovery of Excitability & Reentry
BidirectionalConduction
Mechanism of 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, impulses conduct preferentiallyvia the fast pathway
Initiation of AV Nodal Reentrant Tachycardia
PAC = premature atrial complex (beat)
PAC
PAC
Sustainment of AV Nodal Reentrant Tachycardia
Rate 150-250beats per min
P waves generatedretrogradely(AV node atria) andfall within orat tail of QRS
P P P P
Sustained AV Nodal Reentrant Tachycardia
Note fixed, short RP interval mimicking r’ deflection of QRS
V1
Orthodromic AV Reentrant Tachycardia
AP
Anterogadeconduction via normal pathway
Retrograde conductionvia accessorypathway (AP)
Initiation of Orthodromic AV ReentrantTachycardia
AVN
Ventricles
Atria
AP
PAC = premature atrial complex (beat)
PAC
Sustainment of Orthodromic AV Reciprocating TachycardiaAtria
AP
AVN
Ventricles
Retrograde P’s fall in the ST segmentwith fixed, short RP
Rate 150-250beats per min
Accessory Pathway with Ventricular Preexcitation(Wolff-Parkinson-White Syndrome)
Fusion activation of the ventricles
“Delta” Wave
APPR < .12 s
QRS .12 s
Sinusbeat
Hybrid QRS shape
Varying Degrees of Ventricular Preexcitation
Normal synchronousoverlapping activationof both ventricles:
On timeAsynchronous
scenario I:
Late
Head startOn time(or late)
Asynchronous scenario II:
QRS
Narrow
Wide
Wide
QRS Width: Synchronous vs. Asynchronous Ventricular Activation
Intermittent Accessory Pathway Conduction
NormalConduction
V Preex 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 wavesin the ST segment
Concealed Accessory Pathway
No Delta wave during NSR(but AP capable of retrogradeconduction)
Sinusbeat
Summary of AV Junctional Summary of AV Junctional Reentrant TachycardiasReentrant Tachycardias
Reentrant circuit incorporates AV nodal Reentrant circuit incorporates AV nodal tissuetissue
P waves generated retrogradely over a P waves generated retrogradely over a fast pathwayfast pathway
Short, fixed RP intervalShort, fixed RP interval
Clinical Significance of AV Clinical Significance of AV Junctional Reentrant Junctional Reentrant
TachycardiasTachycardiasRarely life-threateningRarely life-threatening
However, may produce serious symptoms However, may produce serious symptoms (dizziness or syncope [fainting])(dizziness or syncope [fainting])
Can be very disruptive to quality of lifeCan be very disruptive to quality of life
Involvement of an accessory pathway can Involvement of an accessory pathway can carry extra riskscarry extra risks
Atrial Tachyarrhythmias
Sinus Tachycardia (100 to 180+ beats/min)
• P waves oriented normally• PR usually shorter than at rest
Causes of Sinus TachycardiaCauses of Sinus Tachycardia
Hypovolemia ( blood loss, dehydration)Hypovolemia ( blood loss, dehydration)
FeverFever
Respiratory distressRespiratory distress
Heart failureHeart failure
HyperthyroidismHyperthyroidism
Certain drugs (e.g., bronchodilators)Certain drugs (e.g., bronchodilators)
Physiologic states (exercise, excitement, Physiologic states (exercise, excitement, etc)etc)
V5
P P P P’ P
Timing of Expected P
Premature Atrial Complex (PAC)
Non-Compensatory Pause
Premature Atrial Complex (PAC):Premature Atrial Complex (PAC): Alternative Terminology Alternative Terminology
Premature atrial Premature atrial contractioncontraction
Atrial Atrial extrasystoleextrasystole
Atrial Atrial premature beatpremature beat
Atrial Atrial ectopic beatectopic beat
Atrial Atrial prematurepremature depolarizationdepolarization
PACs: Bigeminal Pattern
P P’ P P’ P P’
• Note deformation of T wave by the PAC
• “Regularly Irregular” Rhythm
PACs with Conduction Delay/Block
Physiologic AV Block
PhysiologicAV Delay
Recovered AV Conduction
P
P
P
P’
P’
P’
PAC with “Aberrant Conduction”(Physiologic Delay in the His Purkinje System)V1
P P P’ P
RBBB
V1
PACs with Aberrant Conduction(Physiologic RBBB and LBBB)
RBBB LBBB Normalconduction
PACs with Physiologic LBBB and His-Purkinje System Block
V1
Non-conductedPAC
Non-Conducted PAC
P P PP’
V5
V1
Note deformation of T wave by the PAC
Bigeminal/Blocked PACs Mimicking Sinus Bradycardia
V1
Only the 4th bigeminal PAC conducts
Clinical Significance PAC’sClinical Significance PAC’s
Common in the general populationCommon in the general population
May be associated with heart diseaseMay be associated with heart disease
Can be a precursor to atrial Can be a precursor to atrial
tachyarrhythmiastachyarrhythmias
• RP intervals can be variable • RP often > PR• (Example slower than more common rate mof 150-250 beats per min)
Atrial Tachycardia
V1
Differs fromAV nodal or AV reentrantSVT
Clinical Significance of Atrial Clinical Significance of Atrial TachycardiaTachycardia
Similar to sequela of AV junctional Similar to sequela of AV junctional reentrant tachycardiasreentrant tachycardias
Must be differentiated from them Must be differentiated from them diagnosticallydiagnostically
Atrial Flutter (“Typical,” Counterclockwise)
Reentrant mechanism
II
V1
Atrial Flutter
4:1 2:1
Classicinverted “sawtooth”flutter wavesat 300 min-1 (best seen inII, III and AVF)
Note variableventricularresponse
Atrial Flutter
2:1Conduction(common)
2:1 & 3:2Conduction
1:1Conduction(rare but dangerous)
V. rate 140-160beats/min
Atrial Fibrillation
Focal firingormultiplewavelets
Chaotic, rapidatrial rate at400-600beats per min
V5
Atrial Fibrillation
• Rapid, undulating baseline (best seen in V1)• Most impulses block in AV node Erratic conduction
V1
Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response
II
Atrial Fibrillation with Rapid Ventricular Response
II
Irregularity may be subtle
Atrial Fibrillation: Autonomic Modulation of Ventricular Response
Baseline
Immediately after exercise
Clinical Significance of Atrial Clinical Significance of Atrial Flutter and FibrillationFlutter and Fibrillation
Causes Causes – Usually occur in setting of heart disease; Usually occur in setting of heart disease;
but sometimes see “lone “ atrial fibrillation but sometimes see “lone “ atrial fibrillation– Hyperthyroidism (atrial fibrillation)Hyperthyroidism (atrial fibrillation)
May acutely precipitate myocardial ischemia May acutely precipitate myocardial ischemia or heart failureor heart failure
Chronic uncontolled rates may induce Chronic uncontolled rates may induce cardiomyopathy and heart failurecardiomyopathy and heart failure
Both can predispose to thromboembolic Both can predispose to thromboembolic stroke, etcstroke, etc
Varying Degrees of Ventricular Preexcitation
Atrial Fibrillation with Rapid Conduction Via Accessory Pathway
Atrial Fibrillation with Third Degree AV BlockV1
V5
Regular ventricular rate reflects dissociated slow junctional escape rhythm
Regular Narrow QRS Tachycardias
Differential Diagnosis of Differential Diagnosis of RegularRegular Narrow QRS (Supraventricular) Narrow QRS (Supraventricular)
Tachycardia Tachycardia Reentrant SVT incorporating AV nodal tissueReentrant SVT incorporating AV nodal tissue– AV nodal reentrant tachycardiaAV nodal reentrant tachycardia– Orthodromic AV reentrant tachycardiaOrthodromic AV reentrant tachycardia
SVT mechanism confined to the atriaSVT mechanism confined to the atria– Sinus tachycardiaSinus tachycardia– Atrial flutterAtrial flutter– Other regular atrial tachycardiasOther regular atrial tachycardias
Short-RP favors AV node-dependent Short-RP favors AV node-dependent reentrant SVTreentrant SVT
Determining AV Nodal Participation in Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal SVT by Transiently Depressing AV Nodal
Conduction Conduction Vagotonic ManeuversVagotonic Maneuvers– Carotid sinus massageCarotid sinus massage– Valsalva maneuver (bearing down)Valsalva maneuver (bearing down)– Facial ice pack (“diving reflex;” for kids)Facial ice pack (“diving reflex;” for kids)
Adenosine (6-12 mg I.V.)Adenosine (6-12 mg I.V.)
If SVT “breaksIf SVT “breaks,” a reentrant mechanism ,” a reentrant mechanism involving the AV node is likelyinvolving the AV node is likely
If atrial rate unchanged, but ventricular rate If atrial rate unchanged, but ventricular rate slowsslows (#P’s > #QRS’s), SVT is atrial in (#P’s > #QRS’s), SVT is atrial in originorigin
SVT Responses to AV Nodal SVT Responses to AV Nodal Depressant ManeuversDepressant Maneuvers
SVT terminationSVT termination– AV nodal reentrant tachycardiaAV nodal reentrant tachycardia– Orthodromic AV reentrant tachycardiaOrthodromic AV reentrant tachycardia
No SVT termination (despite maximal No SVT termination (despite maximal attempts)attempts)– Sinus tachycardiaSinus tachycardia– Atrial flutter or fibrillationAtrial flutter or fibrillation– MostMost atrial tachycardias (a minority are atrial tachycardias (a minority are
“adenosine-sensitive”)“adenosine-sensitive”)
Carotid Sinus Massage
Stimulation of carotid sinus triggers baroreceptorreflex and increased vagaltone, affectingSA 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 TachyarrhythmiasVentricular Tachyarrhythmias
Premature Ventricular Complex Premature Ventricular Complex (PVC):(PVC):
Alternative Terminology Alternative Terminology
Premature ventricular Premature ventricular contractioncontraction
Ventricular Ventricular extrasystoleextrasystole
Ventricular Ventricular premature beatpremature beat
Ventricular Ventricular ectopic beatectopic beat
Ventricular Ventricular premature depolarizationpremature depolarization
Premature Ventricular Complex (PVC)
Compensatory Pause
Normal synchronousoverlapping activationof both ventricles:
On timeAsynchronous
scenario I:
Late
Head startOn time(or late)
Asynchronous scenario II:
QRS
Narrow
Wide
Wide
QRS Width: Synchronous vs. Asynchronous Ventricular Activation
PVCs: Bigeminal Pattern
“Regularly Irregular” Rhythm
Ectopic ventricular activation
Normal ventricular activation
Fusionbeat
Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but 100 bpm)
Sinus acceleration
SANode
Ventricular Focus
ATRIA AND VENTRICLESACT INDEPENDENTLY
AV Dissociation
V1
Ventricular Tachycardia (VT)
• 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 BlockFaster atrial rate
Slower ventricular (escape) rhythm
Note that impulses block anterogradely and retrogradelywithin the AV conduction system
Monomorphic VT
V1
Polymorphic VT
Causes of PVC’s and VTCauses of PVC’s and VT
PVC’s are fairly common in normals but are PVC’s are fairly common in normals but are also seen in the setting of heart diseasealso seen in the setting of heart disease
MonomorphicMonomorphic VT often implies heart VT often implies heart disease, but can sometimes be seen in disease, but can sometimes be seen in structurally “normal” heartsstructurally “normal” hearts
PolymorphicPolymorphic VT can result from myoardial VT can result from myoardial ischemia or conditions that prolong ischemia or conditions that prolong ventricular repolarizationventricular repolarization
Electrolyte derangements, hypoxemia and Electrolyte derangements, hypoxemia and drug toxicity can cause PVC’s and VTdrug toxicity can cause PVC’s and VT
MI Scar-Related Sustained Monomorphic VT Circuit
“Torsade de Pointes”(Polymorphic VT Associated with Prolonged Repolarization)
Clinical Significance of PVC’s Clinical Significance of PVC’s and VTand VT
Can be a tip-off to underlying cardiac, Can be a tip-off to underlying cardiac, respiratory or metabolic disorderrespiratory or metabolic disorder
VT may (but need not invariably) lead to VT may (but need not invariably) lead to hemodynamic collapse or more life-hemodynamic collapse or more life-threatening ventricular tachyarrhythmias, threatening ventricular tachyarrhythmias, increasing the risk of cardiac arrestincreasing 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 Clinical Clues to Basis for Regular Wide QRS Tachycardiafor Regular Wide QRS Tachycardia
REMEMBER: VT does REMEMBER: VT does notnot invariably cause invariably cause hemodynamic collapse; patients may be hemodynamic collapse; patients may be conscious and stableconscious and stable
History of heart disease, History of heart disease, especially priorespecially prior myocardial infarctionmyocardial infarction, suggests VT, suggests VT
Occurrence in a young patient with no Occurrence in a young patient with no known heart disease suggests SVTknown heart disease suggests SVT
12-lead EKG (if patient stable) should be 12-lead EKG (if patient stable) should be obtainedobtained
Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction?
More R-Waves Than P-Waves Implies VT!
II
Artifact Mimicking “Ventricular Tachycardia”
Artifact precedes“VT”
QRS complexes “march through”the pseudo-tachyarrhythmia
Limitations of rate controlLimitations of rate control
Atrial fibrillation still present Atrial fibrillation still present – normal sinus – normal sinus rhythm not restoredrhythm not restored
Careful dose titration requiredCareful dose titration required
Administration with 2 or more rate-control Administration with 2 or more rate-control agents is commonagents is common
Can cause ‘Can cause ‘sick sinus syndrome’ in patients sick sinus syndrome’ in patients with a diseased AV nodewith a diseased AV node