ARRITMIAS VENTRICULARES SOSTENIDAS

ARRITMIAS VENTRICULARES SOSTENIDAS
EN URGENCIAS Dra. Ana Martín Residente de 3º año Dr. Francisco Martín. UCIC Servicio de Cardiologia de Salamanca

¿Y ahora qué…? URGENCIAS
Electrocardiogram of right ventricular outflow tract tachycardia.

OPCIÓN A OPCIÓN B

¿Por qué nos pone tan nerviosos?
% MUERTE CARDIACA SÚBITA VALORES DE PREVALENCIA

TAQUICARDIA DE QRS ANCHO (TCA) TAQUICARDIA VENTRICULAR
ESQUEMA SESIÓN Qué son. Formación Evaluación en URGENCIAS: * Estabilidad Ananmesis. Clínica Exploración física Pruebas complementarias (ECG) Diagnóstico diferencial Algorítmos diagnósticos (ECG) Etiologia TV Tratamiento TV

TV. Qué son. Formación TAQUICARDIA VENTRICULAR…..
Taquicardia de QRS ancho (TCA) (alg excepc) Toda taquicardia de QRS ancho no es ventricular. OJO, ante sospecha de TV + inestabilidad hemodinámica.... PRIMERO TRATAMIENTO (NO DIVAGAR)

80% 5% TV. Qué son. Formación Taquicardia QRS ancho TAQUICARDIA
TAQUICARDIA SUPRAVENTRICULAR 80% TSV CON B. conducción Bloqueo rama en RS Fármacos antiarritmicos Alteraciones iónicas Funcional TSV Vaccesoria ANTIDRÓMICA 5% TAQUICARDIA VENTRICULAR

No todo lo que claramente parece TV...
ARTEFACTOS !!!

Antes de nada… INMEDIATAMENTE!! Lo primero la estabilidad del paciente
TCA. Evaluación en urgencias Antes de nada… Lo primero la estabilidad del paciente UN PACIENTE INESTABLE DEBE SER TRATADO INMEDIATAMENTE!!

** ESTABILIDAD TCA. Evaluación en urgencias
EVALUACIÓN DE SIGNOS VITALES Y EL NIVEL DE CONSCIENCIA ESTABLE: SIN COMPROMISO HEMODINÁMICO. Requiere monitorización continua y reevaluación frecuente (rápido deterioro) LA PRESENCIA DE ESTABILIDAD HEMODINÁMICA ERROR COMÚN PARA CONSIDERAR TSV INAPROPIADO Y POTENCIALMENTE PELIGROSA TERAPIA INESTABLE: COMPROMISO HEMODINAMICO PERO ALERTA Y CON PULSO. HIPOTENSIÓN, ANGINA, INSUFICIENCIA CARDIACA Y ALTERACIÓN DEL NIVEL DE CONSCIENCIA PARADA CARDIACA: INCONSCIENTE Y SIN PULSO CARDIOVERSIÓN ELÉCTRICA URGENTE DIFERENTE CLASIFICACIÓN A LAS ULTIMAS GUIAS Immediate assessments of the patient's vital signs and the level of consciousness are of primary importance [6]. In the discussions that follow, patients are categorized as follows: Stable — This refers to a patient showing no evidence of hemodynamic compromise despite a sustained rapid heart rate. Such patients should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration. The presence of hemodynamic stability should not be regarded as diagnostic of SVT [4,10]. Misdiagnosis of VT as SVT based upon hemodynamic stability is a common error that can lead to inappropriate and potentially dangerous therapy. (See "Pharmacologic interventions" below and see "Uncertain diagnosis" below) [3,4]. Unstable — This term refers to a patient with evidence of hemodynamic compromise, but who remains awake with a discernible pulse. In this setting, emergent synchronized cardioversion is the treatment of choice regardless of the mechanism of the arrhythmia. (See "Unstable patient" below). Findings consistent with hemodynamic instability requiring urgent cardioversion include hypotension, angina,altered level of consciousness, and heart failure. Patients who become unresponsive or pulseless are considered to have a cardiac arrest and are treated according to standard resuscitation algorithms. (See "Overview of advanced cardiovascular life support in adults" and see "Overview of basic cardiovascular life support in adults"). ♥ Presincope ♥ Sincope ALGORITMO DE RCP

Ananmesis- clínica Si pac.estable: etiologia y guiar la terapia
TCA. Evaluación en urgencias Ananmesis- clínica Si pac.estable: etiologia y guiar la terapia EDAD Si más de 35 años: probablemente TV (VPP 85%) TSV más probable en JOVENES (VPP del 70%) OJO!! Si historia familiar de TV ó MCS. HITORIA DE ENFERMEDAD CARDIACA Enfermedad cardiaca estructural, enf. coronaria ó IM previo EL PRIMER EPISODIO DE TAQUICARDIA TRAS IM implica TV Marcapasos ó DAI. Historia arritmológica (la primera vez, ya estudiadas…) TSV si recurre durante más de 3 AÑOS >95% pac. con TQRS ancho e IM previo: TV History — When evaluating the stable patient with a WCT, the following historical features may be help to determine the likely etiology and/or guide therapy: History of heart disease — The presence of structural heart disease, especially coronary heart disease and a previous MI, strongly suggests VT as an etiology [4,7]. In one report, over 95 percent of patients with a WCT and a previous MI had VT [7]. It is also important to establish whether a cardiac arrhythmia has occurred in the past and, if so, whether the patient is aware of the etiology. Presence of a pacemaker or ICD — The patient should be asked about the presence of pacemaker or ICD. Patients are instructed to carry identification cards providing information about such devices, which can facilitate device interrogation. The presence of either a pacemaker or an ICD raises the possibility of a device-associated WCT. (see "Supraventricular tachycardia" abovesee "Supraventricular tachycardia" above). More importantly, the presence of an ICD implies that the patient is known to have an increased risk of ventricular tachyarrhythmias and suggests strongly (but does not prove) that the patient's WCT is VT. (See "General principles of the implantable cardioverter-defibrillator"). Symptoms — Symptoms are not useful in determining the diagnosis, but they are important as an indicator of the severity of hemodynamic compromise. Symptoms are primarily due to the elevated heart rate, associated heart disease, and the presence of left ventricular dysfunction [4,6,7]. Some patients with a WCT have few or no symptoms (palpitations, lightheadedness, diaphoresis), while others have severe manifestations including chest pain or angina, syncope, shock, seizures, and cardiac arrest [6]. Age — A WCT in a patient over the age of 35 years is likely to be VT (positive predictive value 85 percent in one series) [11]. SVT is more likely in younger patients (positive predictive value 70 percent). However, VT must be considered in younger patients, particularly those with a family history of ventricular arrhythmias or premature sudden cardiac death. Duration of the tachycardia — SVT is more likely if the tachycardia has recurred over a period of more than three years [6]. The first occurrence of the tachycardia after an MI strongly implies VT [7].

Ananmesis- clínica Tratamiento farmacológico: SINTOMAS:
TCA. Evaluación en urgencias Ananmesis- clínica Tratamiento farmacológico: Antiarrítmicos. Fármacos que alargan QT Digoxina SINTOMAS: Depende: Frecuencia cardiaca. Duración. Función Ventricular Angina, sincope, shock, convulsiones ó PCR. A veces poco ó ningún síntoma: palpitaciones, mareo, sudoración

ECG Pruebas complementarias Bioquímica: Niveles de fármacos
TCA. Evaluación en urgencia Pruebas complementarias Bioquímica: Ionograma: hipopotasemia. Hipomagnesemia. Hiperpotasemia Enzimas cardiacos. Ojo con la elevación de enzimas en pacientes tras CVE Niveles de fármacos ECG Radiografia

VALORACIÓN ELECTROCARDIOGRAFICA
TCA. Evaluación en urgencia. Pruebas complementarias. VALORACIÓN ELECTROCARDIOGRAFICA Datos básicos: Frecuencia cardiaca Regularidad Eje frontal Anchura QRS Disociación Auriculoventricular: Latidos de captura, fusión, Concordancia precordiales Morfologia precordiales: Complejos QR ECG en ritmo sinusal Morfologia en función V1: positivo: BRDHH, origen V.Izq. negativo: BRIHH, origen V.Dcho

Parámetros basicos Frecuencia cardiaca Regularidad:
TCA. Evaluación en urgencia. ECG Parámetros basicos Frecuencia cardiaca Regularidad: “Warm up” Anchura QRS: Dependerá del origen de la TV QRS> 140 mseg con BRDHH QRS> 160 mseg con BRIHH OJO, Existen TV de QRS más estrecho, origen prox. al SIV Eje frontal T.Ventricular Pared ventricular lateral libre…..QRS muy anchos. Rate — The rate of the WCT is of limited use in distinguishing VT from SVT. When the rate is approximately 150 beats per minute, atrial flutter with aberrant conduction should be considered, although this diagnosis should not be accepted without other supporting evidence. Regularity — VT is generally regular, although slight variation in the RR intervals is sometimes seen. Slight irregularity suggests VT as opposed to most SVTs, which are characterized by uniformity of the RR intervals. When the onset of the arrhythmia is available for analysis, a period of irregularity ("warm-up phenomenon"), suggests VT. More marked irregularity of RR intervals occurs in polymorphic VT and in atrial fibrillation (AF) with aberrant conduction. Origen en el septum ó proximo a él… QRS será menor. Otros factores:Tejido infartado. HTV. Disarray muscular (MCPHT) Width of the QRS complex As depicted in fig 5, the site of origin of the VT plays a role in the width of the QRS complex. When the arrhythmia arises in the lateral free wall of the ventricle sequential activation of the ventricles occurs resulting in a very wide QRS. The QRS complex will be smaller when the VT has its origin in or close to the interventricular septum. Of course other factors also play a role in the QRS width during VT, such as scar tissue (after myocardial infarction), ventricular hypertrophy, and muscular disarray (as in hypertrophic cardiomyopathy). It is of interest that a QRS width of more than 0.14 seconds in right BBB (RBBB) tachycardias and 0.16 seconds during left BBB (LBBB) argues for a VT.4 But a QRS width below such values may occur in VTs having their origin in or close to the interventricular septum. Of course, QRS width is not helpful in differentiating VT from a tachycardia with AV conduction over an accessory AV pathway because such a pathway inserts into the ventricle leading to eccentric ventricular activation and a wide QRS complex (fig 6). TSV con QRS > 0.14 (BRD) o >0.16 (BRI) seg.: BRHH preexistente ancianos con fibrosis sist. de conducción y miocardio ventricular TSV antidrómica con via accesoria TSV y fármacos que enlentecen la conducción: antiarrítmicos IC

OJO! NO TODA QRS muy ancho…
Anchura de QRS OJO! NO TODA QRS muy ancho… 200 mseg. Figure 6: An antidromic circus movement tachycardia with AV conduction over a right sided accessory pathway. The insertion of the accessory pathway in the free wall of the right ventricle results in sequential (right to left) ventricular activation and a wide QRS complex. Taquicardia antidrómica por via accesoria derecha.

¿Y Si el QRS es más estrecho que en RS…?
Anchura de QRS ¿Y Si el QRS es más estrecho que en RS…? Alta probabilidad de TV Solo puede explicarse: origen Ventricular cerca del SIV (más simultanea que en RS). Figure 11: Tachycardia QRS smaller than QRS during sinus rhythm. On the left sinus rhythm is present with a very wide QRS because of anterolateral myocardial infarction and pronounced delay in left ventricular activation. On the right a VT arising on the right side of the interventricular septum results in more simultaneous activation of the right and left ventricle than during sinus rhythm and therefore a smaller QRS complex. Tachycardia QRS more narrow than sinus QRS When during tachycardia the QRS is more narrow than during sinus rhythm a VT should be diagnosed. As shown in fig 11, a very wide QRS is present during sinus rhythm because of sequential activation of first the right and then the left ventricle. During tachycardia the QRS is more narrow. This can only be explained by a ventricular origin close to the intraventricular septum, resulting in more simultaneous activation of the right and left ventricle than during sinus rhythm BRIHH con eje izquierdo Origen en lado derecho de SIV Activación izquierda derecha más simultanea QRS ancho por IM anterolateral extenso y retraso en activación ventricular izquierda

Eje frontal Eje muy negativo
TCA. Evaluación en urgencia ECG Parámetros basicos Frecuencia cardiaca Regularidad: Anchura QRS Eje frontal BRDHH + Eje izq : TV BRIHH + Eje dcho: TV Eje entre -90 y +180 = QRS neg. I, II y en III…..TV Origen APEX…Eje IZQUIERDO (>-30º) Origen BASE…Eje DERECHO. Eje muy negativo QRS axis in the frontal plane The QRS axis is not only important for the differentiation of the broad QRS tachycardia but also to identify its site of origin and aetiology. As shown in fig 7, a VT origin in the apical part of the ventricle has a superior axis (to the left of 30). An inferior axis is present when the VT has an origin in the basal area of the ventricle. Previous work4 showed that the presence of a superior axis in patients with RBBB shaped QRS very strongly suggests VT. This does not hold for an LBBB shaped tachycardia. On the contrary, presence of an inferior axis in LBBB shaped QRS tachycardia argues for a VT arising in the outflow tract of the right ventricle.

TCA. Evaluación en urgencia. Pruebas complementarias. VALORACIÓN ELECTROCARDIOGRAFICA Datos básicos: Frecuencia cardiaca Regularidad Eje frontal Anchura QRS Disociación Auriculoventricular Latidos de captura, fusión Morfologia precordiales: Complejos QR Concordancia precordiales ECG en ritmo sinusal

DE LOS CRITERIOS MÁS ÚTILES!!!!!
TCA. Evaluación en urgencia. ECG Disociación AV DE LOS CRITERIOS MÁS ÚTILES!!!!! Actividad auricular independiente de ventricular (Faur<Fvent) MUY ESPECIFICA PERO POCO SENSIBLE Su ausencia no descarta TV: Puede existir y no ser obvia en ECG. En algunas TV, el impulso V conduce NAV y captura el atrio: CONDUCCIÓN RETROGRADA (30%). Sólo ECG % TV. VT from SVT. It occurs in 20–50% of VT and almost never in SVT. Atrioventricular dissociation may be diagnosed by a changeable pulse pressure, irregular canon A waves in the jugular veins and a variable first heart sound. It often demands long 12 lead ECG recordings and careful ECG analysis. In addition, about 30% of VTs have 1:1 retrograde conduction. In the presence of AV dissociation, one may also observe fusion beats which may result from the fusion of a P wave conducted to the ventricles. AV dissociation — AV dissociation is characterized by atrial activity that is independent of ventricular activity (show ECG 8). In a WCT with AV dissociation, an atrial rate slower than the ventricular rate strongly suggests VT. An atrial rate that is faster than the ventricular rate is seen with some SVTs, such as atrial flutter or an atrial tachycardia with 2:1 AV conduction. In these settings, however, there is a consistent relationship between the P waves and the QRS complexes, so there is not true AV dissociation. While the presence of AV dissociation largely establishes VT as the diagnosis, its absence is not as helpful for two reasons: AV dissociation may be present but not obvious on the ECG. In some cases of VT, the ventricular impulses conduct backwards through the AV node and capture the atrium (referred to as retrograde conduction), preventing AV dissociation [21].

TCA. Evaluación en urgencia. ECG Disociación AV
Ondas P neg en cara inf. CONDUCCIÓN RETROGRADA Figure 3: One to one ventriculo-atrial conduction during VT. The p waves are negative in leads II, III, and avf and follow each QRS complex. Left panel VT; right panel same patient during sinus rhythm. Impide disociación AV

Latidos de fusión Morfologia intermedia Su exitencia en una TQRS ancho es diagnóstica de disociación AV y por tanto de TV. Latidos de captura = latidos Dressler Onda P seguido de complejo QRS normal. Latido de fusión: Impulso SV (con onda P) causa activación ventricular con fusión con el complejo originado en el Ventriculo. Resultado = complejo híbrido Capturas = latidos Dressler Onda P seguido de complejo QRS normal. The following findings are helpful in establishing the presence of AV dissociation. Dissociated P waves — P waves are said to be dissociated if they are not consistently coupled to the QRS complexes, as evidenced by the following: PP and RR intervals are different PR intervals are variable There is no association between P and QRS complexes During a WCT, P waves are often difficult to identify. If P waves are not evident on the surface ECG, direct recordings of atrial activity (eg, with an esophageal lead or an intracardiac catheter) can reveal AV dissociation [22]. Fusion beats — Fusion occurs when one impulse originating from the ventricle and a second supraventricular impulse simultaneously activate the ventricular myocardium. The resulting QRS complex has a morphology intermediate between that of a sinus beat and a purely ventricular complex (show ECG 9). Intermittent fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT. Capture beats — Capture beats, or Dressler beats, are QRS complexes during a WCT that are identical to the sinus QRS complex (show ECG 9). The term "capture beat" implies that the normal conduction system has momentarily "captured" control of ventricular activation from the VT focus. Fusion beats and capture beats are more commonly seen when the tachycardia rate is slower. Latidos de fusión y de captura más f. en TV. lentas

F Figure 4: "Capture" (QRS complexes: 5, 13, and 15) and "fusion" beats (QRS complex number 8) during VT In patients with slow VT rates occasional conduction from atrium to ventricle over the AV node-bundle branch system may happen resulting in "capture" or "fusion" beats (fig 4). Sudden narrowing of a QRS complex during VT may also be the result of a premature ventricular depolarisation arising in the ventricle in which the tachycardia originates, or it may occur when retrograde conduction during VT produces a ventricular echo beat leading to fusion with the VT QRS complex.5 Very rarely, AV dissociation is present in tachycardias other than VT. It may occur in AV junctional tachycardia with BBB after cardiac surgery or during digitalis intoxication

TCA. Evaluación en urgencia. Pruebas complementarias. VALORACIÓN ELECTROCARDIOGRAFICA Datos básicos: Frecuencia cardiaca Regularidad Eje frontal Anchura QRS Disociación Auriculoventricular: Latidos de captura, fusión, Morfologia precordiales: Complejos QR Concordancia precordiales ECG en ritmo sinusal Morfologia en función V1: positivo: BRDHH, origen V.Izq. negativo: BRIHH, origen V.Dcho

BLOQUEOS DE RAMA supraventricular
TCA. Evaluación urgencia. ECG Morfologia QRS precordiales BLOQUEOS DE RAMA supraventricular BRDHH BRIHH V1: Trifásico (RSR)…..TSV

TV con morfologia de BRDHH
TCA. Evaluación urgencia. ECG Morfologia QRS precordiales V1 TV con morfologia de BRDHH OJO!! ORIGEN EN VENTRICULO IZQUIERDO LA ACTIVACIÓN DE IZQUIERDA a DERECHA V1 V1: R ancha (>30ms), R monofásica ó qR V6: R/S < 1……. TV Eje izquierdo frontal V6 Marriott6 described that in RBBB shaped tachycardia, presence of a qR or R complex in lead V1 strongly argued for a ventricular origin of the tachycardia, while a three phasic (RSR) pattern suggested a supraventricular origin. Apart from lead V1, lead V6 can also be very helpful in correctly differentiating RBBB shaped tachycardia. When in V6 the R:S ratio is < 1, a VT is very likely.4 As shown in fig 2B an R:S ratio < 1 in V6 is typically found when there is left axis deviation in the frontal plane. If the axis is inferiorly directed, lead V6 often shows an R:S ratio > 1 (fig 2A). TSV: V1,Trifásico (RSR) _V6, R/S > 1 eje inferior.

TV con morfologia de BRIHH
TCA. Evaluación urgencia. ECG Morfologia QRS precordiales TV con morfologia de BRIHH V1 (V2) inicial QRS positivo> 0.03seg. Muesca en descenso S Intervalo comienzo de y nadir S  0.07 seconds V6 : patron qR…. Alta probab. TV V1 V1 In LBBB shaped VT, lead V1 (and also V2) (fig 8) shows: an initially positive QRS with positivity measuring more than 0:03 seconds; slurring or notching of the downstroke of the S wave; and an interval between the beginning of the QRS and the nadir of the S wave of 0.07 seconds or more.7 When lead V6 shows a qR pattern during LBBB shaped tachycardia, VT is very likely. In SVT with LBBB, lead V1 shows no or minimal initial positivity, a very rapid downstroke of the S wave, and a short interval between the beginning of the QRS and the nadir of the S wave (fig 9). V6 TSV: V1, mínima ó ausencia onda r inicial Rápida bajada de S Corto intervalo al nadir de S

TAQUICARDIA SUPRAVENTRICULAR
mínima ó ausencia de r inicial Rápida bajada de S corto intervalo a nadir de S TAQUICARDIA SUPRAVENTRICULAR Figure 9: SVT with LBBB. In panel A LBBB changes during tachycardia into a narrow QRS following a ventricular premature beat. As described in the text, lead V1 during LBBB clearly shows signs pointing to a supraventricular origin of the tachycardia.

Complejos QR Indicadores de escara en miocardio (IM)
TCA. Evaluación urgencia. ECG Morfologia QRS, complejoQR Complejos QR IM ANTERIOR IM INFERIOR Coumel and colleagues9 called attention to the significance of a QR (but not a QS) complex during a broad QRS tachycardia, showing that their presence indicates a scar in the myocardium usually caused by myocardial infarction. Figure 12 gives an example of QR complexes during VT in patients with an anterior (panel A) and an old inferior myocardial infarction (panel B). QR complexes during VT are present in approximately 40% of VTs after myocardial infarction QRS complexes during VT indicating a myocardial scar. As shown by the accompanying tracing, during sinus rhythm anterior wall myocardial infarction is present in the left panel and inferior wall myocardial infarction in the right one. Indicadores de escara en miocardio (IM) Están presentes en el 40% de las TV despues de IM

Comienzo QRS al nadir de S
TCA. Evaluación urgencia. ECG Comienzo QRS al nadir de S BRUGADA Intervalo RS > 100 ms en  una precordial … altamente sugestivo de TV. OJO: TSV con VAccesoria TSV con fármacos que enlentezcan la conducción intraventricular (flecainida) TSV con BRHH preexistente One should be careful, however, because such a duration may occur in SVT with AV conduction over an accessory pathway, SVT during administration of drugs that slow intraventricular conduction (in particular, flecainide), and in SVT with pre-existent BBB, especially LBBB

TCA. Evaluación en urgencia. Pruebas complementarias. VALORACIÓN ELECTROCARDIOGRAFICA Datos básicos: Frecuencia cardiaca Regularidad Eje frontal Anchura QRS Disociación Auriculoventricular: Latidos de captura, fusión, Morfologia precordiales: Complejos QR Concordancia precordiales ECG en ritmo sinusal

TV APICAL TCA. Evaluación urgencia. ECG Concordancia precordiales
QRS CUANDO SON MONOFÁSICOS Y CON LA MISMA POLARIDAD Si algún complejo es bifásico… ya no existe concordancia Especifidad>90 % Sensibilidad :20% CONCORDANCIA NEGATIVA Todas precordiales NEGATIVAS TV APICAL CONCORDANCIA POSITIVA Todas precordiales POSITIVAS TV TSV con Vacc. izq Activación horizontal comienza en A. posterior While the presence of concordance strongly suggests VT (>90 percent specificity), its absence is not helpful diagnostically (approximately 20 percent sensitivity) [8].negative ECG patterns in the precordial leads—If all precordial leads are predominantly negative, a VT is the likely diagnosis. If all precordial leads are predominantly positive, the differential diagnosis is an antidromic tachycardia using a left sided accessory pathway or a VT. c QRS morphologies in V1 and V6—In an RBBB pattern, a monophasic R wave, a broad (. 30 ms) R, or a qR in V1 strongly suggest VT. A monophasic R wave, or an S greater than an R in V6, also suggest VT. In the presence of an LBBB pattern, a broad R wave (usually greater than 30 ms) and/or a slow descent to the When all precordial leads show either negative or positive QRS complexes this is called negative or positive concordancy. Negative concordancy is diagnostic for a VT arising in the apical area of the heart (fig 10). Positive concordancy means that in the horizontal plane ventricular activation starts left posteriorly. This can be found either in VT originating in the left posterior wall or during tachycardias using a left posterior accessory AV pathway for AV conduction (fig 10).

Concordancia en precordiales
T.V. apical T.V. TSV con Vacc. post izquierda Figure 10: Concordant pattern. The left panel shows a VT arising in the apical area of the left ventricle resulting in negative concordancy of all precordial leads. In the right panel ventricular activation starts in the left posterior area, resulting in positive concordancy of all precordial leads. The latter can be found in left posterior VT but also in SVT with AV conduction over a left posterior accessory pathway

TCA. Evaluación en urgencia. Pruebas complementarias. VALORACIÓN ELECTROCARDIOGRAFICA Datos básicos: Frecuencia cardiaca Regularidad Eje frontal Anchura QRS Disociación Auriculoventricular: Latidos de captura, fusión, Morfologia precordiales: Complejos QR Concordancia precordiales ECG en ritmo sinusal

Valor del ECG en ritmo sinusal
BRIHH preexistente. Pre-excitación Infato de miocardio antiguo Alteraciones conducción AV en RS :TV QRS más ancho que TCA : TV The ECG during sinus rhythm may show changes such as pre-existent BBB, ventricular pre-excitation, or an old myocardial infarction which are very helpful in correctly interpreting the ECG during broad QRS tachycardia. Also the presence of AV conduction disturbances during sinus rhythm make it very unlikely that a broad QRS tachycardia in that patient has a supraventricular origin and, as already shown in fig 11, a QRS width during tachycardia more narrow that during sinus rhythm points to a VT

MUCHOS DATOS ECG….PERO NINGUNO SUFICIENTEMENTE
ESPECÍFICO NI SENSIBLE PARA FACILITAR EL DIAGNÓSTICO DE TV

ALGORITMOS DIAGNÓSTICOS ECG ÚTILES… (unos más que otros…)

“El típico”: algoritmo de BRUGADA
NO CONCORDANCIA “El típico”: algoritmo de BRUGADA Velocidad inicial más lenta que la final

TAQUICARDIA VENTRICULAR Varón 81 años POSITIVO EN V1
MORFOLOGIA BRDD monofásica ORIGEN EN VENTRICULO IZQ. TAQUICARDIA VENTRICULAR 81 yr. old male with ventricular tachycardia NO HAY CONCORDANCIA NO FUSIÓN/CAPTURA

2007 Vereckei A Eje sup. dcho. No rS Velocidad inicial más lenta
Capacidad diagnóstica mayor que los criterios de Brugada (P = 0.006) Mayor S y VPN (-) en TV, mayor E y VPP para TSV [VPN para TV y VPP para TSV: 83.5% new vs Algoritmo Brugada Eje sup. dcho. 2007 Vereckei A No rS Velocidad inicial más lenta que la final Vereckei et al. propose, and nicely demonstrate, two new criteria for differentiating between ventricular and supraventricular origins of WCT. The first criterion is the presence of a positive and dominant R wave in lead aVR, and the second is based on the vi:vt ratio. The rationale for these criteria is eminently reasonable. A QRS axis that is deviated to the right superior quadrant has long been recognized as being caused by VT, and this phenomenon is similar to an R wave in lead aVR.1 The criterion based on the vi:vt ratio is also simple and reasonable. SVT not associated with structural cardiac disease or drug presence, for example, would be expected to show rapid initial forces and delayed mid-terminal forces.2 Derivación bifásica ó multifásica

TAQUICARDIA VENTRICULAR Varón 81 años
81 yr. old male with ventricular tachycardia The need for rapid, accurate diagnosis in patients who present with WCTs is critical, both to identify the most appropriate acute therapeutic intervention and to establish the prognosis and long-term therapy. In this paper, Vereckei et al. propose, and nicely demonstrate, two new criteria for differentiating between ventricular and supraventricular origins of WCT. The first criterion is the presence of a positive and dominant R wave in lead aVR, and the second is based on the vi:vt ratio. The rationale for these criteria is eminently reasonable. A QRS axis that is deviated to the right superior quadrant has long been recognized as being caused by VT, and this phenomenon is similar to an R wave in lead aVR.1 The criterion based on the vi:vt ratio is also simple and reasonable. SVT not associated with structural cardiac disease or drug presence, for example, would be expected to show rapid initial forces and delayed mid-terminal forces.2

TAQUICARDIA SUPRAVENTRICULAR vi/vt is .1 (0.85/ 0.4 in lead V5
V6: 110mseg. POR BRUGADA, TAQUICARDIA VENTRICULAR

Algoritmo aVR (2008) Vereckei A
Presencia de R inicial Anchura de r ó q inicial >40mseg. Muesca en descenso inicial del QRS predominantemente negativo Activación ventricular, razón de velocidades (Vi/Vt). Voltaje de primeros 40mseg(Vi)/ voltaje ultimos 40mseg(Vt) del QRS Cuando existe presencia de uno de los criterios de 1 a 3, la TV es diagnosticada. Si están ausentes, se analiza el criterio 4: Vi/Vt>1 sugiere TSV, y Vi/Vt ≤1 sugiere TV New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. 3rd Department of Medicine, Semmelweis University, Budapest, Hungary. BACKGROUND: We recently reported an ECG algorithm for differential diagnosis of regular wide QRS complex tachycardias that was superior to the Brugada algorithm. OBJECTIVE: The purpose of this study was to further simplify the algorithm by omitting the complicated morphologic criteria and restricting the analysis to lead aVR. METHODS: In this study, 483 wide QRS complex tachycardias [351 ventricular tachycardias (VTs), 112 supraventricular tachycardias (SVTs), 20 preexcited tachycardias] from 313 patients with proven diagnoses were prospectively analyzed by two of the authors blinded to the diagnosis. Lead aVR was analyzed for (1) presence of an initial R wave, (2) width of an initial r or q wave >40 ms, (3) notching on the initial downstroke of a predominantly negative QRS complex, and (4) ventricular activation-velocity ratio (v(i)/v(t)), the vertical excursion (in millivolts) recorded during the initial (v(i)) and terminal (v(t)) 40 ms of the QRS complex. When any of criteria 1 to 3 was present, VT was diagnosed; when absent, the next criterion was analyzed. In step 4, v(i)/v(t) >1 suggested SVT, and v(i)/v(t) </=1 suggested VT. RESULTS: The accuracy of the new aVR algorithm and our previous algorithm was superior to that of the Brugada algorithm (P = .002 and P = .007, respectively). The aVR algorithm and our previous algorithm had greater sensitivity (P <.001 and P = .001, respectively) and negative predictive value for diagnosing VT and greater specificity (P <.001 and P = .001, respectively) and positive predictive value for diagnosing SVT compared with the Brugada criteria. CONCLUSION: The simplified aVR algorithm classified wide QRS complex tachycardias with the same accuracy as standard criteria and our previous algorithm and was superior to the Brugada algorithm. PMID: [PubMed - in process] Lead aVR was analyzed for (1) presence of an initial R wave, (2) width of an initial r or q wave >40 ms, (3) notching on the initial downstroke of a predominantly negative QRS complex, and (4) ventricular activation–velocity ratio (vi/vt), the vertical excursion (in millivolts) recorded during the initial (vi) and terminal (vt) 40 ms of the QRS complex. When any of criteria 1 to 3 was present, VT was diagnosed; when absent, the next criterion was analyzed. In step 4, vi/vt >1 suggested SVT, and vi/vt ≤1 suggested VT.

TAQUICARDIA VENTRICULAR Varón 81 años aVR Presencia de R inicial
Anchura de r ó q inicial >40mseg. Muesca en descenso inicial del QRS neg. Activación ventricular(Vi/Vt). aVR 81 yr. old male with ventricular tachycardia Cuando existe presencia de uno de criterios de 1 a 3, TV

Diagnóstico de TQRS ancho en PREEXCITACIÓN

TAQUICARDIA VENTRICULAR QR> 100mseg ActV. ventricular
Presencia de R inicial Anchura de r ó q inicial >40mseg. Muesca en descenso inicial del QRS neg. Activación ventricular(Vi/Vt). Morfologia típica BRIHH Eje izquierdo No disociación QR> 100mseg An antidromic circus movement tachycardia with AV conduction over a right sided accessory pathway. The insertion of the accessory pathway in the free wall of the right ventricle results in sequential (right to left) ventricular activation and a wide QRS complex. ActV. ventricular (Vi/Vt) < 1

EEF: Taquicardia antidrómica por via accesoria derecha.
An antidromic circus movement tachycardia with AV conduction over a right sided accessory pathway. The insertion of the accessory pathway in the free wall of the right ventricle results in sequential (right to left) ventricular activation and a wide QRS complex.

Etiología 80% <5% 10-15% Sin cardiopatia estructural
MIOCARDIOPATIAS Reentrada por cicatriz miocardica: Infarto. Changas. Sarcoidosis. Postquirúgica. Congénticas. … Escara de fibrosis densa ocasiona áreas de bloqueo de la conducción. Fibrosis entre miocitos disminuye el acoplamiento celular, distorsiona la propagación, enlenteciendo la conducción, promoviendo fenómenos de reentrada

Etiologia TV: Con cardiopatia estructural: “Ritmo idioventricular acelerado” Taquicardia rama-rama Displasia arritmogénica de V.derecho Sin cardiopatia estructural: TV idiopatica TSVderecho TV idiopatica izquierda Síndrome QT largo Sindrome QT corto Síndrome de Brugada

RITMO IDIOVENTRICULAR ACELERADO
VARÓN DE 55 AÑOS QUE ACUDE POR DOLOR TORÁCICO SIN ACTIVIDAD SINUSAL NORMAL Frecuencia: 82lpm MORFOLOGIA BRIHH FIGURA 33 Interpretation: The QRS rhythm is regular at a rate of about 82/minute. The QRS complexes are not preceded by P waves. The mean frontal plane axis of the QRS complexes is about +60°, and their duration is about 200 msec (best seen in the precordial leads). The origin of the QRS rhythm may be in the AV junction, with associated intraventricular aberration, or in fascicular or ventricular tissue. In the setting of AMI, the latter is more likely. Notches deform the end of the QRS complexes (best seen in leads I, aVL, V1, and V5-6). These notches might be P waves, or part of the QRS complexes themselves. If they are P waves, they occur in 1:1 relationship to the QRS complexes; inability to discern their configuration in leads II, III, and aVF makes it difficult to ascertain whether they represent retrograde atrial depolarization. Careful measurement of the QRS duration in the leads in which it is clearest indicates that the notches are in fact part of the QRS complexes and not P waves; no underlying atrial rhythm is discerned. The QRS complexes have an LBBB pattern, but because ventricular depolarization may not be occurring over the normal AV node His-Purkinje pathway, definitive statements about underlying intraventricular conduction delay cannot be made. ST-segment elevation is present in leads II, III, and aVF, and ST-segment depression in leads I, aVL, and V5-6. A diagnosis of myocardial ischemia or infarction cannot be made with certainty in the presence of a left intraventricular conduction delay. In the setting of AMI, this rhythm could indicate either reperfusion or reperfusion injury. Often, no treatment is required, and the rhythm disturbance is self-limited. RITMO IDIOVENTRICULAR ACELERADO

Taquicardia reentrada rama-rama
Pacientes con IC. IM anteroseptal Miocardiopatia dilatada idiop. Distrofia miotónica. Post cirugía valvular aórtica Traumatismo torácico ant. Circuito de reentrada (hiss-purkinje) Morfologia BRIHH. Eje normal ó izquierdo ~ TSV con aberración. Disociación AV ABLACIÓN con RF de rama derecha de HH. This type of re-entry may occur in patients with anteroseptal myocardial infarction, idiopathic dilated cardiomyopathy, myotonic dystrophy, after aortic valve surgery, and after severe frontal chest trauma.

Morfologia BRIHH Eje izquierdo
LA MISMA MORFOLOGIA QUE EN RITMO SINUSAL Bundle Branch Reentrant VT

DAVD eje BRIHH ORIGEN: APEX V.DCHO MORFOLOGIA: BRIHH EJE IZQUIERDO
DISPLASIA ARRITMOGÉNICA DE VENTRICULO DERECHO. Figure 15: VT in arrhythmogenic right ventricular dysplasia (ARVD). VT shows LBBB shape and left axis deviation indicating an origin in the apex of the right ventricle. Note also the negative T waves in V1-V3 during sinus rhythm, which is often found in ARVD Vi/Vt

DAVD, en ritmo sinusal Twelve lead electrocardiogram in a patient with arrhythmogenic right ventricular dysplasia showing deep T wave inversions in V2 to V4, compatible with right ventricular disease, and epsilon waves just after the QRS complex (arrows). Data from Jaoude, S, Leclercq, JF, Coumel, P. Eur Heart J 1996; 17:1717.

T. V. Idiopática (TSVdcho.)
JOVENES (♀) Morfologia de BRIHH eje dcho. Mecanismo: actividad desencadenada postpotenciales tardios (AMPc). Desencadenadas con esfuerzo Bien toleradas. Función ventricular normal. Buen ptco. Rta. a betabloqueantes, sotalol, bloqueantes de canales Ca. ABLACIÓN CON RADIOFRECUENCIA. TV. morfologia BRIHH CON EJE IZQUIERDO …. sospecha de DAVD. (tb T. mediada por VA Mahaim) TVTSVDCHO extremadamente IMPROBABLE TV. MORFOLOGIA DE BRIHH CON EJE IZQUIERDO …. SOSPECHA DE DAVD. (tb T. mediada por VA Mahaim) TVTSVDCHO EXTREMADAMENTE IMPROBABLE Idiopathic ventricular outflow tract tachycardia This arrhythmia usually originates in the right ventricular outflow tract and manifests as a left bundle branch block VT with an inferior axis (fig 7). It is often seen in younger patients (female . male) without structural heart disease and accounts for up to 70% of idiopathic VT. Although the majority of cases appear to occur sporadically rather than on a familial basis, the condition is generally considered as a ‘‘primary electrical disease’’. It is important in the differential diagnosis of various entities, in particular mild or subclinical forms of arrhythmogenic right ventricular cardiomyopathy.8 Most data suggest that the underlying mechanism is triggered activity caused by adenylcyclase-mediated delayed afterdepolarisations. Idiopathic outflow tract tachycardias are usually exertion or stress related arrhythmias. They can also present as recurrent extrasystoles or non-sustained arrhythmias tending to occur at rest, or provoked only with exercise (Gallavardin’s tachycardias). However, these forms may just represent different spectra of the same arrhythmia. Idiopathic outflow tract tachycardias are usually well tolerated, probably because of the preserved ventricular function. Hence, this VT has a favourable long term prognosis when compared with VT in structural heart disease. The arrhythmia is often responsive to treatment with b blockers, sotalol9 or calcium channel blockers and can also be amenable to transcatheter ablation.8 10 In ARVD there are three predilection sites in the right ventricle: the inflow and outflow tracts, and the apex. While the first two sites have a QRS configuration during tachycardia which is difficult to differentiate from right ventricular idiopathic VT, left axis deviation in a young person with an LBBB shaped VT should immediately lead to the suspicion of ARVD. In fact, there is an important rule in LBBB shaped VT with left axis deviation that cardiac disease should be suspected and that idiopathic right ventricular VT is extremely unlikely

TV. MORFOLOGIA DE BRIHH CON EJE IZQUIERDO …. SOSPECHA DE DAVD. (tb T. mediada por VA Mahaim) TVTSVDCHO EXTREMADAMENTE IMPROBABLE Idiopathic ventricular outflow tract tachycardia This arrhythmia usually originates in the right ventricular outflow tract and manifests as a left bundle branch block VT with an inferior axis (fig 7). It is often seen in younger patients (female . male) without structural heart disease and accounts for up to 70% of idiopathic VT. Although the majority of cases appear to occur sporadically rather than on a familial basis, the condition is generally considered as a ‘‘primary electrical disease’’. It is important in the differential diagnosis of various entities, in particular mild or subclinical forms of arrhythmogenic right ventricular cardiomyopathy.8 Most data suggest that the underlying mechanism is triggered activity caused by adenylcyclase-mediated delayed afterdepolarisations. Idiopathic outflow tract tachycardias are usually exertion or stress related arrhythmias. They can also present as recurrent extrasystoles or non-sustained arrhythmias tending to occur at rest, or provoked only with exercise (Gallavardin’s tachycardias). However, these forms may just represent different spectra of the same arrhythmia. Idiopathic outflow tract tachycardias are usually well tolerated, probably because of the preserved ventricular function. Hence, this VT has a favourable long term prognosis when compared with VT in structural heart disease. The arrhythmia is often responsive to treatment with b blockers, sotalol9 or calcium channel blockers and can also be amenable to transcatheter ablation.8 10 In ARVD there are three predilection sites in the right ventricle: the inflow and outflow tracts, and the apex. While the first two sites have a QRS configuration during tachycardia which is difficult to differentiate from right ventricular idiopathic VT, left axis deviation in a young person with an LBBB shaped VT should immediately lead to the suspicion of ARVD. In fact, there is an important rule in LBBB shaped VT with left axis deviation that cardiac disease should be suspected and that idiopathic right ventricular VT is extremely unlikely

TV. morfologia BRIHH CON EJE derecho y transición tardia en precordiales Figura 1: Electrocardiograma donde se observa el padrón típico de un TV idiopática de VD. Tipo bloqueo de rama izquierda con eje eléctrico hacia arriba. Al tener aVL predominantemente negativo sugiere un origen en la región septal del tracto de salida de ventrículo derecho

Varón de 39 años. Palpitaciones intermitentes. No sincope ó presíncope.
TAQUICARDIA VENTRICULAR TRACTO DE SALIDA (eje inferior) VENTRICULO DERECHO EJE DERECHO MORFOLOGIA BRIHH BIGEMISNIMO FIGURA 28 Interpretation: The rhythm in the first three panels is regular at a rate of about 120/minute, and the QRS complexes measure about 120 msec in duration. Their mean frontal plane axis is about +80°. Notches in the T waves, signifying atrial depolarizations, are present in 1:1 relationship to the QRS complexes. The P waves are inverted in leads II, III, and aVF, indicating that atrial depolarization is occurring retrogradely. The origin of this QRS rhythm cannot be known with certainty, and may be supraventricular with intraventricular aberration, junctional, or ventricular. A junctional tachycardia is somewhat unusual in this age group, and, because the QRS complexes are not narrow and normal-appearing, intraventricular aberration would have to be present. The rhythm is more likely originating in ventricular tissue. Because the mean frontal plane QRS axis of the tachycardia complexes is inferiorly directed, the focus of origin is at or near the base of the ventricle, with ventricular depolarization proceeding from base to apex. Because in the precordial leads the QRS complexes have an LBBB pattern, the focus of origin is likely the RV. In the last portion of the third panel, the ventricular tachycardia terminates, and normal sinus rhythm spontaneously resumes. The QRST complexes of the sinus-conducted beats are normal. Ventricular bigeminy is present, likely originating from the same focus as the tachycardia. Many of these tachycardias are benign, and occur in the absence of structural heart disease. They are often amenable to cure by radiofrequency ablation. Conducción retrograda

Electrocardiogram of ventricular tachycardia arising from the left sinus of Valsalva. Note the prominent broad R wave in leads V1 and V2.

PATRONES DE TSVDcho B, Eje QRS:inferior I, negativo ORIGEN: SEPTAL
TSVDdcho A Eje QRS:+70 I, positivo ORIGEN: LATERAL TSVDdcho Figure 13: Three types of idiopathic VT arising in or close to the outflow tract of the right ventricle (see text). Figure 13 shows three patterns of idiopathic VT arising in or close to the outflow tract of the right ventricle. All three have an LBBB-like QRS complex indicating a right ventricular origin. In panel A the frontal QRS axis is +70 and lead 1 shows a positive QRS complex, indicating an origin of the tachycardia in the lateral part of the outflow tract of the right ventricle. In panel B the frontal QRS axis is inferior and the QRS is negative in lead 1, pointing to an origin on the septal side in the right ventricular outflow tract. In panel C an inferior frontal QRS axis and QRS negativity in lead 1 are also present, but leads V1 and V2 clearly show initial positivity of the QRS complex. This is a tachycardia not arising on the endocardial surface of the right ventricular outflow tract but epicardially in between the root of the aorta and the posterior part of the outflow tract of the right ventricle. It is important to recognise this pattern because this site of origin of the VT cannot be treated with catheter ablation in contrast to the tachycardias depicted in panel A and B C, Eje QRS:inf. I, negativo V1, V2, inicialmente + ORIGEN: epicardio entre techo de aorta y parte posterior TSVDdcho No ablación con RF

T.V. IDIOPÁTICA izq. JÓVENES ♂ SIN ENFERMEDAD CARDIACA. MECANISMO DE REENTRADA ó actividad desencadenada Prox. septum cerca del fasciculo posterior en Vent. Izq. QRS relativamente estrecho (0.10 a 1.14). MORFOLOGIA DE BRDHH EJE SUPERIOR IZQUIERDO (eje noreste). PRONÓSTICO BUENO, a.v. muy sintomáticos. Frecuente respuesta a VERAPAMILO No a Betabloqueantes. ABLACIÓN con EF terapia curativa en sintomáticos. Similar a BRD + HBA Idiopathic left ventricular tachycardia (fascicular VT) Idiopathic left ventricular tachycardia (ILVT) tends to occur in young, predominantly male patients without structural heart disease.11 The arrhythmia has a relatively narrow (0.10– 0.14 s) RBBB morphology with a rapid downstroke of S waves in the precordial leads and a left superior axis (fig 8). ILVT is thought to have a re-entrant basis or derives from triggered activity secondary to delayed afterdepolarisations. It arises on or near to the septum near the left posterior fascicle. Rarely, VT can arise from the left anterior fascicle and thus produce an RBBB pattern with right axis deviation. These VT are often unresponsive to b blockers, but frequently respond to verapamil (‘‘verapamil sensitive’’ VT). The prognosis is generally good, but these patients may be highly symptomatic. Catheter ablation (fig 8)12 offers curative therapy and should be considered early in the management of symptomatic patients.

TAQUICARDIA IDIOPATICA FASCICULAR
EJE IZQUIERDO MORFOLOGIA BRDHH

TSVIzquierdo TAQUICARDIA IDIOPATICA FASCICULAR
ORIGEN CERCA DE FASCICULO ANTERIO. MORFOLOGIA BRDHH EJE DERECHO They all have an RBBB shape because of an origin in the left ventricle. The most common type is shown in panel A. The frontal QRS axis shows left axis deviation. The site of origin of the VT is in or close to the posterior fascicle of the LBB. In panel B the frontal QRS axis is further leftward (a so called north-west axis). This tachycardia arises more anteriorly close to the interventricular septum. The least common idiopathic left VT is the one shown in panel C. Now the frontal QRS axis is inferiorly directed. This VT originates in the anterior fascicle of the LBB. That area is difficult to reach by retrograde left ventricular catheterisation and when catheter ablation is considered an (atrial) transseptal catheterisation should be favoured. In ARVD there are three predilection sites in the right ventricle: the inflow and outflow tracts, and the apex. While the first two sites have a QRS configuration during tachycardia which is difficult to differentiate from right ventricular idiopathic VT, left axis deviation in a young person with an LBBB shaped VT should immediately lead to the suspicion of ARVD. In fact, there is an important rule in LBBB shaped VT with left axis deviation that cardiac disease should be suspected and that idiopathic right ventricular VT is extremely unlikely TRATAMIENTO CON ABLACIÓN MÁS COMPLEJO, VÍA TRASEPTAL.

Síndrome de QT largo . 1. Key clinical characteristics of inherited long QT syndrome (LQTS) are shown, including prolongation of QT interval on electrocardiogram (ECG), commonly associated arrhythmia (torsades de pointes), clinical manifestation, and long-term outcomes. NPV=negative predictive value; PPV=positive predictive value; QTc=corrected QT interval.

Síndrome de QT largo

Síndrome de QT largo alargamiento de QT PAUSA QT prolongado basalmente
GURE Polymorphic ventricular tachycardia with the features of torsade de pointes. Note the baseline QT prolongation, with abrupt lengthening of the QT interval after the pause, followed by the onset of polymorphic ventricular tachycardia, which suddenly terminates.

Síndrome de QT corto Intervalo QTc < 320 ms (otros, 270)
Síndrome NUEVO asociado a MUERTE CARDIACA SÚBITA Sin ENFERMEDAD CARDIACA ESTRUCTURAL Prevalencia desconocida. A cualquier edad Historia familiar de MCS, sincope, ó P. cardiaco por TV polimorfica Intervalo QTc < 320 ms (otros, 270) Tratamiento: quinidina (alarga QT). DAI

Síndrome de QT corto QT: 240mseg QTc:290mseg
ECG from a 71 year old patient with a short QT syndrome and atrial fibrillation (QT interval 240 ms, QTc 290 ms, paper speed 25 mm/sec).

T.V. polimórfica catecolaminérgica
JOVENES. Sin cardiopatia estructural. AF: 1/3pac. MCS súbita ó síncope con stress 40-60% mutaciones en dos canales de Calcio Sincope, ó MCS en rta. stress físico ó emocional ECG: TV bidireccional, TV polimórfica, FV idiopática Mortalidad alta 30-50% a los 30 años Tratamiento: beta bloqueantes, calcioantagonistas, antiarrítmicos ó DAI

T.V. polimórfica catecolaminérgica
Taquicardia bidireccional con ejercicio en un paciente con TV polimórfica

S. BRUGADA ENTIDAD CLÍNICA CARACTERIZADA POR UNA ELEVACIÓN DEL SEGMENTO ST EN V1- V3 Y MORFOLOGÍA DE BRD EN EL ECG ASOCIADAS A SÍNCOPE Y MUERTE SÚBITA CARDIACA Síndrome de muerte súbita nocturna inesperada (SUNS); Sudeste asiático Bangungut (“levantarse y lamentarse en sueños”); Filipinas Pokkuri (“fenómeno de cese brusco e inesperado”); Japón Lai Tai (“muerte durante el sueño”) # 58% de los pacientes con S. Brugada, origen asiático

SÍNCOPE DEFECTO GENÉTICO (SCN5A) PAREJA Evs MUERTE CARDIACA SÚBITA
ANOMALIA ELÉCTRICA PRIMARIA EPICARDIO VENTRÍCULO DCHO TIPO 1 ECG (“COVED”) PAREJA Evs TAQUICARDIA VENTRICULAR POLIMÓRFICA TV/FV AUTOLIMITADA SÍNCOPE FV SOSTENIDA MUERTE CARDIACA SÚBITA

PATRÓN ECG European Society of Cardiology TIPO I TIPO II TIPO III

LA COMUNIDAD MÉDICA DEBE RECONOCER EL PATRÓN ECG, POR SU IMPORTANTE REPERCUSIÓN
JOVENES MUERTE SÚBITA NOCTURNA GURE Dynamic nature of the electrocardiographic pattern associated with Brugada syndrome. Left: Nondiagnostic J point elevation in precordial leads V1 and V2. Right: Diagnostic coved ST-segment elevation in both leads following the administration of 1 g procainamide. CORAZÓN “SANO”

Tratamiento TV. INESTABLE TV ESTABLE FÁRMACOS CVE
Cardioversión eléctrica inmediata TV ESTABLE FÁRMACOS CVE

TV inestable CV ELÉCTRICA SINCRONIZADA 50-100 J. de E. Bifásica
MALA TOLERANCIA: Hipotensión Angina Insuficiencia cardiaca CV ELÉCTRICA SINCRONIZADA J. de E. Bifásica Tratamiento Si la taquicardia ventricular (TV) sostenida se asocia a hipotensión, insuficiencia cardiaca aguda, disnea o angor, está indicada la cardioversión inmediata. Se sedará al paciente. La cardioversión deberá realizarse en modo “sincronizado” para minimizar el riesgo de que degenere en fibrilación ventricular. Deberemos asegurarnos de que las palas del desfibrilador estén bien colocadas (paraesternal derecha y sobre la punta del corazón). No hacerlo así predispone a que las descargas sean inefectivas. Es relativamente frecuente ver que, durante la “histeria colectiva” que rodea a veces a una situación de parada cardiaca, la pala esternal se coloca en el epigastrio y la precordial en el flanco izquierdo (se está cardiovertiendo el “bazo” en lugar de el corazón). Si el paciente no tiene pulso externo y ha perdido la consciencia, se aplicará una energía de cardioversión de 200 julios y luego se continuará con 300 julios si persiste la TV. Si las circunstancias son menos dramáticas, se puede realizar una cardioversión sincronizada inicial de 50 ó 100 julios, seguida de energías progresivamente mayores si las medidas iniciales no dan resultado. Si la TV mantenida se tolera bien y no existen dudas del origen ventricular de la misma, se puede intentar cardiovertirla con fármacos antiarrítmicos. La lidocaína es eficaz en las TV que se presentan durante la fase aguda del infarto de miocardio (ver dosis en el apéndice final). La procainamida es más efectiva que la lidocaína, y también es muy útil en las TV no asociadas a isquemia aguda (miocardiopatías, infartos antiguos, etc.). La amiodarona intravenosa y el sulfato de bretilio mejoran la eficacia de la desfibrilación. Si la TV mantenida es bien tolerada por el paciente y existen dudas razonables del origen ventricular de la arritmia por el contexto clínico del enfermo y el registro electrocardiográfico, se debe establecer contacto con la Unidad Coronaria/UCI para el ingreso inmediato o para la reversión eléctrica mediante sobreestimulación o extraestímulos, previa colocación de un catéter en la aurícula derecha para establecer el diagnóstico etiológico de la taquiarritmia aberrada. El tratamiento posterior de la taquicardia ventricular será el ingreso hospitalario en Cardiología para la valoración del tipo de tratamiento más adecuado dependiendo del tipo y tolerancia de la TV, la cardiopatía subyacente, la forma de presentación y la fracción de eyección (FE) del ventrículo izquierdo. Es imprescindible que el enfermo ingrese en una Unidad con Monitorización ECG Continua (sala con telemetría o, en su defecto, en la Unidad Coronaria/UCI). Se sedará al paciente. “Sincronización” para evitar degeneración en FV. Colocación correcta de palas paraesternal derecha y sobre la punta del corazón EVITAR la “histeria colectiva” 50 ó 100 julios, post. E. mayores. Si no se sincroniza: Emax. Sin pulso externo/consciencia 200 J

TV estable. fármacos Si la TV mantenida se tolera bien y no existen dudas del origen ventricular , CV fármacos antiarrítmico: PROCAINAMIDA AMIODARONA LIDOCAINA POSTERIORMENTE: INGRESO EN CARDIOLOGIA/ UNIDAD CORONARIA DIAGNÓSTICO ETIOLÓGICO, CARDIOPATIA SUBYACENTE, FUNCIÓN VENTRICULAR…… TRATAMIENTO ÓPTIMO.

TV estable. Fármacos. PROCAINAMIDA
VIAL de 10 ml, con 1000mg Dosis de carga: 15-18 mg/kg (1gr.) infusión lenta en 30 min. Bolos de mg, repitiendo cada 5 minutes hasta que cese ó 1gramo. Reducir dosis de carga12 mg/kg si IRenal ó Disfunción cardiaca Dosis de mantenimiento: 1-4 mg/min. Reducir 1/3 de dosis si IR ó IC moderada Reducir 2/3 en IR grave ó disfunción cardiaca grave STOP: control arrítmico. Hipotensión. Ensanchamiento de QRS de más del 50%. Dosis máxima de 17 mg/kg Ampollas de Amiodarona: 150mg/3ml. Preparación: 150mg en G5% 250ml. No utilizar envases de PVC. Ampollas de Procainamida: 1g/10ml. Preparación: Inducción sin diluir, Mantenimiento: 1g en G5% 250ml. Ampollas de Lidocaina: 1%=100mg/10ml. 5%=2’5g/50ml. Preparación: Inducción sin diluir, Mantenimiento: 1g en G5% 250ml. Procainamida (Biocoryl®): viales de 10 mL que contienen mg. Es el fármaco de primera elección TV sostenidas no relacionadas con isquemia miocárdica aguda. La dosis iniciales, en situaciones urgentes, con la administración de 10 mg/kg de peso ( mg) disueltos en 100 cc de suero fisiológico a pasar en 5-10 minutos. Si la situación lo permite, puede administrarse más despacio, en forma de bolo de 100 mg disueltos en 10 cc de suero fisiológico a pasar en dos minutos y repetidos cada cinco minutos, hasta que se termine la arritmia, se alcance una dosis máxima de 1 g o aparezcan efectos secundarios (ensanchamiento del QRS <25%). Puede continuarse con una dosis de mantenimiento de 2-4 mg/minuto (2.000 mg en 480 mL de suero glucosado al 5% a razón de mL/hora, respectivamente). No debe prescribirse en situación de hipotensión arterial (excepto en la RCP), pues puede agravarla. También puede provocar molestias gastrointestinales y alteraciones sobre el SNC similares a las causadas por la lidocaína, pero de menor intensidad. Ensancha el QRS y alarga el QT.

TV estable. fármacos Amiodarona Lidocaina VIAL 50mL 5%:2,5g
VIAL 10mL 1%:100mg/ VIAL de 3ml, con 150mg Amiodarona BOLO de 150 mg (or 5 mg/kg) IV en 10 minutos; Perfusión de 360 mg (1 mg/min) en 6 h mg (0.5 mg/min) 18 h. Dosis máxima (incluyendo bolos) is 2.2 gramos/24h Lidocaina Bolo de 0.5 to 0.75 mg/kg; repetido cada 5 a 10 minutos como sea necesario. Al mismo tiempo, perfusion :1 a 4mg/min Dosis máxima total de 3 mg/kg en una hora Lidocaína: se administra en viales de 2 mL y 10 mL al 2% (2 mL que contienen 40 mg; 10 mL que contienen 200 mg). El frasco de 500 mL tiene un contenido de mg (2%). La dosis inicial es de 1 mg/kg de peso en bolo iv, y se continúa con una infusión iv inicial de 3-4 mg/minuto durante las primeras horas, para después disminuir, si es posible, a una dosis de 1-2 mg/minuto (de la solución al 2%: 15 mL/hora equivalen a 1 mg/minuto). En el caso de infarto agudo de miocardio, si transcurren 12 horas sin recidiva de la arritmia de base y el paciente la recibe a 1-2 mg/minuto, puede suspenderse. Si la arritmia o el riesgo potencial persisten, se mantendrá la administración a 2-3 mg/minuto, según la tolerancia y con monitorización continua del ritmo cardiaco. En los pacientes con más de 70 años o con insuficiencia cardiaca o con insuficiencia hepatocelular impor-tante, debe mantenerse a 2 mg/minuto. En los casos de bajo gasto cardiaco importante, a 1 mg/minuto. Puede provocar excitación del SNC, convulsiones, estupor y confusión, sobre todo si el paciente cumple los criterios de riesgo antes mencionados. En Urgencias, hemos vivido cuadros confusionales agudos tras administrar mg de lidocaína, con gran agitación psicomotriz, que han cedido espontáneamente en minutos con amnesia del episodio. A dosis altas, puede deprimir la conducción A-V y presentar un efecto inotrópico negativo. En nuestro laboratorio, se consideran valores terapéuticos los comprendidos entre 6,4 y 25,6 mmol/L. Pueden ser solicitados con carácter urgente.

TV polimórfica. Magnesio (Sulmetin®) 1’5g/10ml (1 Amp) en 2-3 min.
2-20 mg/min (4’5 g en 250 ml: 6-60 ml/h) Taquicardizar MP externo. Isoproterrenol:1mg perfusión(5 amp 250ml: 3-300ml/h) Evitar fármacos que acortan el QT. VIAL de 10mL: 1,5g Ampolla de magnesio: 1.5g en 10 ml. Preparación: Inducción sin diluir, Mantenimiento: 4g en G5% ó SF 250ml. Ampolla de Isoproterrenol: 0.2mg/1ml. Preparación: 1mg en G5% 250ml. VIAL de 1ml, con 0,2 mg

CONCLUSIONES (TCA) ANTE UNA TAQUICARDIA DE QRS ANCHO… NO TEMBLAR!!
EVALUA LA SITUACIÓN HEMODINÁMICA BUSCA SIGNOS ECG SISTEMÁTICA/ (disociación AV…) SÍ DISPONIBLE ANALIZA EL ECG en Ritmo sinusal TEN EN CUENTA QUE ESTADÍSTICAMENTE TV es MUCHO MÁS COMUN QUE LA TSV (TQRS ancho) NUNCA COMETAS EL ERROR DE RECHAZAR UNA TV por que el enfermo permanezca hemodinamicamente estable CUANDO DUDES, NO ADMINISTRES VERAPAMILO Do not panic when confronted with a broad QRS tachycardia. Look for clinical signs of AV dissociation and evaluate the 12 lead ECG systematically (see box above). Also, when available, look at the 12 lead ECG during sinus rhythm. This approach usually gives the correct diagnosis of VT versus SVT. Keep in mind that statistically VT is much more common than SVT in the broad QRS tachycardia. Never make the mistake of rejecting VT because the broad QRS tachycardia is haemodynamically well tolerated. When in doubt, do not give verapamil or adenosine; procainamide should be used instead

Último ECG… ¿qué opinais? ¿TV?
ESTÁ A LA MITAD DE VELOCIDAD, a 100lpm QRS ESTRECHO TIENE ONDAS P EXTRASISTOLIA SUPRAVENTRICULAR

TAQUICARDIA VENTRICULAR “RESUCITA” CON APOCAR
TRATAMIENTO No precisa Revisión por cardiologia Emconcor 5mg, un comp. Orfidal 1mg

Dra. Ana Martín Residente de 3º año Dr. Francisco Martín. UCIC
'Quick! Give me the paddles!' Dra. Ana Martín Residente de 3º año Dr. Francisco Martín. UCIC Servicio de Cardiologia de Salamanca

Dra. Ana Martín Residente de 3º año Dr. Francisco Martín. UCIC
Servicio de Cardiologia de Salamanca

ARRITMIAS VENTRICULARES SOSTENIDAS

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ARRITMIAS VENTRICULARES SOSTENIDAS

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