DIAGNOSTICO ECG DE LAS TAQUICARDIAS CON QRS ANGOSTO

Presentación del tema: "DIAGNOSTICO ECG DE LAS TAQUICARDIAS CON QRS ANGOSTO"— Transcripción de la presentación:

1 DIAGNOSTICO ECG DE LAS TAQUICARDIAS CON QRS ANGOSTO

2 TAQUICARDIAS CON QRS ANGOSTO
Ritmo irregular Fibrilación auricular Flutter auricular con conducción variable Taquicardia atrial multifocal o ritmo auricular caótico

3 TAQUICARDIAS CON QRS ANGOSTO
Ritmo regular RP<PR reentrada intranodal típica (<70mS) reentada AV ortodrómica (>70mS)

4 TAQUICARDIAS CON QRS ANGOSTO
Ritmo regular RP>PR Taquicardia sinusal Taquicardia atrial automática Taquicardia unional reciprocante permanente (Coumel) RIN atípica

5 TAQUICARDIAS AURICULARES
Focales Taquicardia sinusal inapropiada Por macroreentrada Aleteos auriculares típicos (horarios o antihorarios) Aleteos auriculares atípicos Taquicardias auriculares incisionales Fibrilación auricular

6 Taquicardia Sinusal inapropiada y secundaria
In Sinus Tachycardia, the EKG deflection will show a normal P and R-wave depolarization, with a rapid tachycardic rate Sinus Tachycardia rates range between BPM The underlying Mechanism for Sinus Tachycardia is Abnormal Automaticity (Hyper-Automaticity) Origen: Nodo Sinusal Frecuencia: LPM Mecanismo: Automaticidad Anormal (Hiper) Disautomomía

7 Reentrada Reentry refers to an electrical impulse continuously traveling an electrical loop within the myocardium. The depolarization wave-front reenters areas that have just been repolarized, creating a circular, continuous series of depolarizations and repolarizations. The following anatomic and physiologic properties create a reentrant loop: Two parallel conduction pathways around a central obstacle (A and B in above figure). Conducting tissue connects the pathways at both ends. One of the pathways (A) conducts more slowly than the other The other pathway, (B), exhibits unidirectional block, usually in the form of a substantially longer refractory period than the other pathway

8 Substrato + Gatillo = Reentrada
To put it briefly: The tissue that forms the block and pathways for a reentry circuit is called the substrate A premature impulse (such as a Premature Ventricular Contraction, or PVC) serves as a trigger Substrate + Trigger results in reentry *Note: A substrate may develop due to scar tissue from various forms of heart disease. Substrato + Gatillo = Reentrada

9 Reentrada For reentry to occur, the following events must take place:
A premature impulse occurs in the reentrant circuit at a time when Pathway A (with the short refractory period) is ready to accept the impulse, and Pathway B (with the long refractory period) is still repolarizing from the previous depolarization. The impulse slowly travels through Pathway A and reaches Pathway B just as Pathway B completes it repolarization and is no longer refractory, which means it is ready to accept a stimulus. The impulse travels through Pathway B in a retrograde direction and reenters Pathway A. The impulse is conducted antegrade through Pathway A, and the circuit continues. Reentry does not display a “warm up” or “cool down” period.

10 REENTRADA INTRANODAL Figure Typical and atypical atrioventricular node reentrant tachycardia (AVNRT). Typical atrioventricular (AV) node reentry is shown in A. An impulse from the atrium enters the AV node and travels down both the slow and fast pathway. It quickly travels down the fast pathway resulting in activation of the ventricles with a short PR interval and results in the blocking of the impulse from the slow pathway when it reaches the terminal portion of the AV node since the tissue is still refractory. An atrial premature depolarization (APD) results in the conduction of the impulse down the slow pathway and thus longer PR interval. It blocks in the fast pathway since that tissue has a longer refractory period. If the tissue of the fast pathway regains conduction, the impulse after traveling down the slow pathway can return retrogradely back to the atrium via the fast pathway resulting in an atrial echo beat. A key component of the circuit is that the retrograde impulse finds the fast pathway no longer refractory. For this to occur, there must be a suitable delay in antegrade conduction over the slow pathway. The QRS complex is narrow because the ventricle is being activated via the normal HPS. Retrograde activation over the fast pathway happens quickly, and on the surface electrocardiogram, the retrograde P wave is usually "buried" or at the tail end of the QRS complex. This can give the appearance of a "pseudo" right bundle branch pattern in lead V1. This is a short-RP tachycardia. -slow pathway; -fast pathway; NSR-normal sinus rhythm; SVT-supraventricular tachycardia. (Courtesy of Harlan R. Grogin.)

11 Taquicardia AV por Reentrada Nodal
Origen: Nodo AV Mecanismo: Reentrada Frecuencia: 150 – 230 LPM, más rápida en los adolescentes Características: QRD Normal con ausencia de ondas P; en la TSV más común en adultos This is a reentrant supraventricular rhythm whose reentry circuit is located in the region of the atrioventricular node. It is characterized by a QRS morphology that is normal for the patient. The rate of AVNRT is commonly between BPM, and can exceed 250 BPM in teenagers. Note that on the EKG, P-waves are unseen and are usually buried in the QRS. Approximately 60% of narrow-complex tachycardias are found to be caused by AVNRT. Here are some other characteristics of AVNRT: A paroxysmal onset and termination is seen with AVNRT. There is both a typical and atypical form of AVNRT. Typical AVNRT is a result of a shift in conduction from the fast to the slow pathway, and is seen in 90% of the patients with AVNRT. Atypical AVNRT is a result of a conduction shift from the slow to fast or slow to the slow pathway. The atypical form is less common, occurring in 10% of the patients with AVNRT. AVNRT is not associated with underlying heart disease. It may present at any age, but usually occurs in the mid 40s, and may be more frequent in females. AVNRT appears to be catecholamine sensitive, as there are increased episodes reported with exercise, emotional stress, and use of caffeine. The frequency of AVNRT episodes can be from once every 2 or 3 years to several times a day.

12 Fibrilación Atrial (FA)
* Animación Origen: Aurícula Derecha y/o Izquierda Mecanismo: Múltiples ondas de reentrada Frecuencia: 400 LPM Características: Ritmo caótico y aleatorio; Tremor Auricular; asociado con ritmo ventricular irregular Atrial Fibrillation (AF) is characterized by random, chaotic contractions of the atrial myocardium. Patients have an atrial rate of 400 BPM or more, often too fast to measure on an EKG. A surface EKG shows atrial fibrillation as irregular, wavy deflections (fibrillatory waves) between narrow QRS complexes. The fibrillatory waves vary in shape, amplitude, and direction. The chaotic nature of atrial fibrillation results in a grossly irregular ventricular rhythm. The rhythm is considered controlled if the ventricular rate is less than 100 BPM; uncontrolled if the ventricular rate conducts to greater than 100 BPM. Mechanism: In AF, the multiple wavelets of reentry do not allow the atria to organize. The ectopic focus or foci are said to be located around or within the pulmonary veins. Drugs such as flecainide, sotalol and amiodarone can terminate and prevent atrial fibrillation. Drug therapy can be used before or after DC cardioversion to maintain sinus rhythm after cardioversion.

13 Fibrilación Atrial (FA)
The primary mechanism of atrial fibrillation is thought to be multiple wavelet reentry. It occurs when adjacent cells in the atrial myocardium have different refractory periods (uneven recovery times). During multiple wavelet reentry: An electrical impulse passing through the atrial myocardium depolarizes excitable cells and moves around refractory cells The rerouted electrical impulse then stimulates any adjacent cells that have recovered their excitability By this time, the cells first stimulated are again excitable. The electrical impulse re-excites the cells and continues to move through the atria, exciting and re-exciting the cells it encounters Unlike a normal depolarization wave that travels from cell to cell in one direction, reentry waves wander across the myocardium, randomly splitting off and following different reentrant pathways (see illustration). This random movement causes the chaotic, uncoordinated contractions of atrial fibrillation.

14 Porque la FA engendra más FA
Mecanismo de la FA Porque la FA engendra más FA Los episodios frecuentes o prolongados de FA pueden causar FA crónica o permanente debido a que: Producen periodos refractarios progresivamente más cortos permitiendo la reentrada de ondas que se auto propagan y se difunden Electrical Remodeling is thought to be responsible for the progression of atrial fibrillation. It shortens the wavelength of an atrial impulse and allows more reentry wavelets to coexist in the atria at a given time. The electrical remodeling effect is often called AF begets AF. It works like this: When AF episodes are frequent or long, the refractory periods of myocardial cells become progressively shorter This increases the excitable periods of myocardial cells and gives reentry waves more opportunities to self-propagate (spread). The more wavelets present in the atria, the less likely they will self-extinguish. This increases the duration of an AF episode and decreases the likelihood AF will self-terminate or respond to cardioversion. Note: Increased atrial size due to underlying cardiovascular disease may contribute to an increased number of wavelets that can coexist in the atria.

15 Otros Mecanismos de la FA
Disparos multifocales Atrial fibrillation can also result from the rapid discharge of impulses from one or many ectopic (non-sinus) sites in the atria. The ectopic cells (called foci) depolarize independently of the sinus node and disrupt the normal sinus rhythm. Multifocal firing takes place at multiple atrial ectopic sites. The cells produce many depolarization waves that activate different areas of the atrial myocardium at different times. AF occurs because the myocardial cells do not contract and relax rhythmically, in normal synchronization with the sinus node. *Note: Because a mechanism of AF may be Mulifocal Firing, some would argue that AF is a disorder of Impulse Formation (abnormal automaticity), rather than Impulse Conduction (multiple wavelets of reentry). Some argue still that while ectopic or mulifocal firing may begin AF, it is reentry that sustains it. For purposes of laying out rhythm disorders in this presentation, AF has been identified as a disorder of Impulse Conduction due to how it is sustained. May it be understood, however, that it could arguably be classified under both disorder descriptions. Mecanismo: Automaticidad anormal (multi-sitio) Características: Muchas ondas de Desporalización; la activación ocurre asincrónicamente; no está en ritmo con el Nodo Sinusal

16 Otros Mecanismos de la FA
Disparos en un solo foco Single focus firing is the rapid discharge of electric impulses from a single atrial ectopic site. A common site of single focus firing is the posterior left atrium, near the pulmonary veins. Mecanismo: Automaticidad anormal (monofocal, usualmente en la parte posterior de la Aurícula Izquierda) Características: Descarga rápida; un solo foco ectópico

17 Flutter o Aleteo Atrial
* Animación Atrial flutter produces an atrial rate between 250 and 400 BPM. The ventricular rate may increase, but it is always slower than the atrial rate. During atrial flutter, atrial impulses are conducted to the ventricles in various ratios. Even conduction ratios (2:1, 4:1) are more common than odd ratios (3:1, 5:1). In a 2:1 ratio, there are two flutter waves for every QRS complex. A constant conduction ratio (e.g., 2:1) results in a regular ventricular rhythm (most common). A variable ratio (e.g., 4:1 to 2:1 to 5:1) results in an irregular ventricular rhythm. Origen: Aurícula Derecha & Izquierda Mecanismo: Reentrada Características: Ondas P rápidas y regulares

18 FLUTTER AURICULAR

19 Flutter inverso

20 Flutter o taquicardia incisional

21 Wolff-Parkinson-White
Origen: Fuera del Nodo AV Mecanismo: Reentrada Frecuencia: 180 – 260 LPM. Puede ser más rápida Características: Intervalo PR corto (< 120 ms), QRS ancho (> 110 ms), Onda Delta Obvia y notoria WPW is characterized by: Short PR interval (120 ms or less) indicating that the impulse did not travel the path through the AV Node. QRS is wide (110 ms or greater) again implying the impulse did not travel through the normal conduction system; and An obvious delta wave as a result of early conduction. A delta wave looks like a gradual onset of the QRS complex (above graphic) and the QRS is >110 ms. The PR interval is typically less than 120 ms. As mentioned, the most common SVT in WPW is orthodromic, which creates a narrow complex QRS. Approximately 7%-10% of WPW is antidromic, which creates a wide complex QRS (exaggeration of delta wave).

22 Wolff-Parkinson-White
Vía Accesoria = Haz de Kent Ortodrómica - 90% - Nodo AV – conducción anterógrada; - Vía Extra – conducción retrógrada Antidrómica – 10% - Vía extra – conducción anterógrada - Nodo AV – conducción retrógrada Wolff-Parkinson-White Syndrome is one cause of AVRT. The impulse travels through an extra pathway formed by tissue called the Bundle of Kent, located in the right or left atrium. The AV node is bypassed. Orthodromic WPW uses the AV node for antegrade conduction and the accessory pathway for retrograde conduction. Most patients who have WPW Syndrome exhibit this conduction pattern, which results in a narrow complex tachycardia with P-waves following the QRS complex. Antidromic WPW exists when antegrade conduction is via the bypass tract, and the retrograde return via the AVN. Only 10% or less of WPW patients will have this conduction pattern, which results in a wide, bizarre, complex tachycardia.

23 AVRT * Ortodrómica Mecanismo: Reentrada
Animación Vía Accesoria Here is an example of the mechanism of reentry with patients having an A to V accessory pathway. The extra pathway serves as one limb of the reentry circuit. Fast conduction properties A relatively slower refractory period. The second limb of the circuit is the normal AV conduction pathway. Conducts slowly, recovers quickly. A tachycardia can be started by an appropriately timed premature atrial or ventricular beat. Should it occur when the pathway is in refractory, it will be conducted to the ventricles via normal AV conduction. If the impulse travels in the retrograde direction, the extra pathway may have recovered, conducting the impulse back to the atrium. This tachycardia is referred to as orthodromic (seen on the next slide), as the conduction travels antegrade through the AV node. The retrograde path is via the accessory pathway. Mecanismo: Reentrada Frecuencia: 180 – 260 LPM. Algunas veces más rápida Características: Una vía eléctrica accesoria o extra hacia los ventrículos. Se lo conoce más comúnmente como Síndrome de Wolff-Parkinson-White (WPW)

24 AVRT * Antidrómica Mecanismo: Reentrada
Animación Vía Accesoria Antidromic Tachycardia — proceeds in the reverse direction; a wide QRS tachycardia except when the accessory pathway is located in the right anteroseptal location very close to the His bundle. When multiple pathways are present, it is also possible for the circuit to use 2 pathways as a circuit. Mecanismo: Reentrada Frecuencia: 180 – 260 LPM. Algunas veces más rápida Características: Una vía eléctrica accesoria o extra hacia los ventrículos, que produce una taquicardia de complejos anchos

25 Taquicardia Auricular multifocal
Atrial Tachycardia is defined as a series of 3 more consecutive atrial premature beats occurring at a rate of >100 BPM. Atrial tachycardia is usually paroxysmal (PAT – Paroxysmal atrial tachycardia), it starts and ends abruptly. It can occur in healthy as well as diseased hearts and may result from emotional stress or excessive use of alcohol, tobacco, or caffeine. Origin: Ectopic focus located in the atrium Mechanism: Abnormal Automaticity Origen: Aurícula – Foco Ectópico Frecuencia: >100 LPM Mecanismo: Automaticidad Anormal

26 TAQUICARDIAS CON QRS angosto
Figure Electrocardiographic patterns of narrow complex tachycardias. The most important clue to the mechanism of a narrow complex tachycardia is the relationship of the P wave to the QRS complex. No visible P wave often means that the P wave is buried in the QRS complex. This is usually due to typical atrioventricular (AV) nodal reentry. With typical AV nodal reentry, the P wave may also be located just at the start or end of the QRS complex, giving a qRs or Rsr' pattern. When the P wave is located close to the previous QRS complex, it is identified as a short-RP tachycardia. This is often seen with accessory pathway-mediated tachycardia and is due to retrograde atrial activation over the accessory pathway. The P wave may also be far from the previous QRS complex and classified as a long-RP tachycardia. If the P wave is inverted, it may be the result of atypical AV node reentry, or it may be using a slowly conducting accessory pathway in the retrograde direction. AVNRT-atrioventricular nodal reentry tachycardia; ECG-electrocardiogram. (Courtesy of Harlan R. Grogin.)

27 GRACIAS