Narrow QRS Tachycardia

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Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.

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  • Figure 2. Main Mechanisms and Typical Electrocardiographic Recordings of Supraventricular Tachycardia. In patients with atrioventricular (AV) nodal reentrant tachycardia (Panels A and B), the atrioventricular node is functionally divided into two pathways that form the reentrant circuit. In the majority of patients, during this type of tachycardia, antegrade conduction to the ventricle occurs over the slow pathway and retrograde conduction over the fast pathway. The activation of atria and ventricles is synchronous so that the retrograde P wave is buried in the QRS complex, or it may be visible soon after the QRS complex (as pseudo r&apos; in V1 or pseudo s in the inferior leads). Orthodromic AV reentrant tachycardia (Panels A and B) is the most frequent arrhythmia in patients who have an accessory pathway, with antegrade conduction through the AV node, activation of the ventricles, and retrograde conduction through the accessory pathway. Typically, there is a short RP interval, but a long RP interval may be associated with slow-conducting accessory pathways. With the use of adenosine or vagal maneuvers (Panel C), tachycardia often terminates with a retrograde P wave. In the approximately 70 percent of patients with this type of tachycardia who have an obvious accessory pathway, preexcitation may be seen in the ensuing beats; however, it is absent in the approximately 30 percent of patients with a concealed accessory pathway. In antidromic AV reentrant tachycardia (Panels A and B), the activation wave front travels in the opposite direction. On electrocardiography, it is impossible to distinguish antidromic AV reentrant tachycardia from ventricular tachycardia. Atrial tachycardias (Panels A and B) typically have a focal origin (star), and different mechanisms might be involved (reentry within several millimeters, automaticity, and triggered activity). RP intervals are typically long (longer than PR intervals), but this depends on the rate of tachycardia and properties of AV conduction. The PR interval can be prolonged by the use of vagal maneuvers and adenosine (Panel C), which may also produce a transient AV block. A substantial proportion of focal atrial tachycardias are terminated with the use of adenosine. Atrial flutter with 2:1 AV conduction (Panels A and B) may resemble atrial tachycardia or another type of supraventricular tachycardia and can be revealed when vagal maneuvers or adenosine is used (Panel C).
  • Figure 2. Diagram of AV nodal reentrant tachycardia (AVNRT). The electrical impulse travels in a circle using extra fibers in and around the AV node.
  • Figure 3. A diagram of AV reentrant tachycardia (AVRT). The electrical impulse travels down the AV node to the ventricles and back to the atrium via extra fibers that connect the atria and ventricles.
  • Figure 3. Algorithm for the Short-Term Management of Supraventricular Tachycardia (SVT). If the diagnosis of SVT with aberration or SVT with preexcitation is not certain, tachycardia with a wide QRS complex must be considered as an unknown mechanism and treated as such. SVT with preexcitation can be the result of either antidromic atrioventricular reentry or, uncommonly, another type of SVT (e.g., atrial tachycardia) with an accessory pathway that is not critical for the maintenance of the arrhythmia. BBB denotes bundle-branch block, VT ventricular tachycardia, IV intravenous, and ECG electrocardiogram. Adapted from Blomstrom-Lundqvist et al.8
  • Figure 4. Algorithm for the Long-Term Management of Supraventricular Tachycardia. In many circumstances, patient preference is an important consideration in the selection of therapy. Referral to an electrophysiologist should be considered for discussion of the risks and benefits of catheter ablation.
  • Narrow QRS Tachycardia

    1. 1. DR.PRANAV,DM(Cardiology) NIMS,Hyderabad-500082,India NARROW QRS TACHYCARDIA
    2. 2. SVTs from a sinoatrial source: Inappropriate sinus tachycardia (IST) Sinoatrial nodal reentrant tachycardia (SNRT) SVTs from an atrial source: Ectopic (unifocal) atrial tachycardia (EAT) Multifocal atrial tachycardia (MAT) Atrial fibrillation with a rapid ventricular response Atrial flutter with a rapid ventricular response Without rapid ventricular response, fibrillation and flutter are usually not classified as SVT SVTs from an atrioventricular source (junctional tachycardia): AVNRT or junctional reciprocating tachycardia (JRT) Permanent (or persistent) junctional reciprocating tachycardia (PJRT), a form of JRT which occurs predominantly in infants and children but can occasionally occur in adults AV reciprocating tachycardia (AVRT) - visible or concealed (including Wolff-Parkinson-White syndrome) Junctional ectopic tachycardia (JET)
    3. 3. In brief Response to carotid sinus massage or adenosine –with termination of arrhythmia with Pwave –AVNRT with atrial premature beat . Tachycardia persists with AV block –AT,AFL,SANRT Pseudo r ‘ wave in V1 –AVNRT SHORT RP interval – AVNRT,AVRT Long RP interval – AT,SANRT,AVNRT atypical
    4. 4. ECG findings
    5. 5. Main Mechanisms and Typical Electrocardiographic Recordings of Supraventricular Tachycard
    6. 6. AVNRT Presence of a narrow complex tachycardia with regular R-R intervals and no visible p waves. P waves are retrograde and are inverted in leads II,III,AVF. P waves are buried in the QRS complexes –simultaneous activation of atria and ventricles – most common presentation of AVNRT –66%. If not synchronous –pseudo s wave in inferior leads ,pseudo r’ wave in lead V1---30% cases . P wave may be farther away from QRS complex distorting the ST segment ---AVNRT ,mostly AVRT.
    7. 7. AV NODAL REENTRANT TACHYCARDIA
    8. 8. AVRT Typical – RP interval < PR interval RP interval > 80 milli sec Atypical –RP interval > PR interval Concealed bypass tract – only retrograde conduction Manifest bypass tract– both anterograde and retrograde. Electrical alternans –the amplitude of QRS complexes varies by 5 mm alternatively. Rate related BBB occuring and the rate of tachycardia is decreasing –then the bypass tract is on the same side of the block.
    9. 9. AV REENTRANT TACHYCARDIA
    10. 10. WPW syndrome Two types Orthodromic Antidromic Antidromic is wide complex tachycardia In NSR detected by delta wave. Can ppt into AF and VF on use of AV nodal blockers MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe. CONCEALED WPW syndrome – no delta wave .less risk of AF
    11. 11. Orthodromic AVRT
    12. 12.  Short PR interval  Normal QRS complex  PSVT
    13. 13. Sinus Tachycardia
    14. 14. Focal Atrial Tachycardia P wave morphology changes. PR interval > 0.12 sec . Second,third degree AV block can occur. Tachycardia terminates with a qrs complex .. Right atrial origin– p wave inverted in V1. If biphasic in V1—initially positive then negative. Upright in lead AVL Opposite if of left atrial origin Superior origin –upright p waves in inferior leads Inferior origin –p waves are inverted in inferior leads.
    15. 15. Focal atrial tachycardia (LA focus)
    16. 16. Multifocal Atrial Tachycardia At least three consequtive p waves with different morphologies with a rate > 100 bpm to be present. Isoelectric baseline between p waves. Also called as choatic atrial tachycardia Mostly seen in COPD ,electrolyte abn,theophylline Rate usually does not exceed 130-140 bpm.
    17. 17. Multifocal Atrial Tachycardia
    18. 18. SANRTMicroreentrant tachycardia Usually precipitated and terminated by premature atrial complexes. Atrial rate is usually 120-150 bpm. IART - Large or small reentrant circuit. AV block can occur.
    19. 19. Junctional tachycardias Non paroxysmal – accelerated junctional rhythm Rate < 100 bpm Usually junctional node 40-60 bpm Paroxysmal or focal junctional tachycardia is rare – automaticity. 110-250bpm. P waves may be before or after QRS complex Infrequent and nonsustained episodes –no treatment Acute termination of SVT and establish the mechanism of SVT in case of acute setting. Long term goal is abolishing the arryhthmia substrate. Precipitating factors – electrolyte imbalance,hypoxia,ischemia,hyperthyroidism to be sought out.
    20. 20. Thank you reading this.

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