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Tachycardia Approach and Management

Tachycardia Approach and Management

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Publicado porChadi Alraies
Palpitations and tachycardia are common problems in all age groups, young and old populations. The patient usually presents with shortness of breath and palpitations or sometimes can be settled and the only presentation is fatigue or generalized weakness.

In this lecture I am going to go with you over the type of tachycardia and how to differentiate between each type and what is the appropriate management at the bedside and by the expert.

It is going to be helpful for all people in the medical fields, nurses, paramedics, physician assistants, and doctors in training or in practice.

Please feel free to let me know if you have any comments or additions.

Thank you
Palpitations and tachycardia are common problems in all age groups, young and old populations. The patient usually presents with shortness of breath and palpitations or sometimes can be settled and the only presentation is fatigue or generalized weakness.

In this lecture I am going to go with you over the type of tachycardia and how to differentiate between each type and what is the appropriate management at the bedside and by the expert.

It is going to be helpful for all people in the medical fields, nurses, paramedics, physician assistants, and doctors in training or in practice.

Please feel free to let me know if you have any comments or additions.

Thank you

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Published by: Chadi Alraies on Sep 10, 2009
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M Chadi Alraies, MD Cleveland Clinic Foundation

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The initial step in management of all patients with tachycardia is to evaluate for hemodynamic instability:

Is the patient experiencing signs and symptoms related to the rapid heart rate?

Hypotension, dyspnea, decreased level of

consciousness, chest pain, shock

If hemodynamically unstable, often no time for ECG and thorough evaluation

If stable, 12-lead ECG can be used to differentiate

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Narrow or Wide Complex? < 120 msec = narrow > 120 msec = wide

Narrow complex tachycardias reflect synchronous activation of both ventricles via supraventricular initiation, ie sinus node,

atria, AV node, His bundle

Wide complex tachycardias (WCTs) may be

ventricular in origin, SVT with aberrant
conduction, or accessory pathway mediated

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SVT with aberrancy:

Widening of the QRS complex due to delayed or blocked conduction in the HisPurkinje system, ie preexisting or ratedependent RBBB or LBBB with superimposed sinus or atrial tachycardia, Afib/flutter

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I. Wide Complex Tachycardia
Is it VT or SVT with aberrancy?  VT is most common cause of WCT, up to 80%1-4  When evaluating the patient with WCT, cannot exclude VT due to presence of hemodynamic stability  Misdiagnosis of VT as SVT and subsequent use of AV nodal blocking agents (CCBs, beta blockers, adenosine) may precipitate VF – ie, coronary steal due to adenosine  DC cardioversion is treatment of choice for unstable WCTs

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How do we differentiate between VT and SVT with aberrancy?
History is important:  Presence of structural heart disease, especially previous MI strongly suggestive of VT (greater than 98% in one report5).  Age: greater than 35, more likely VT – PPV 85%; under 35 more likely SVT – PPV 70%6.  Is there a history of arrhythmia, or is the patient on antiarrhythmic or other cardiac meds?

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Physical Exam:

 

Does the patient have a pacemaker, an ICD, or a sternotomy scar? AV dissociation may cause cannon A waves of JVP: intermittent and irregular pulsations of greater than normal amplitude resulting from simultaneous atrial and ventricular contraction. Contraction of RA against closed TV produces transient increase in RA and JVP Highly inconsistent fluctuations in BP due to variability in the degree of LA contribution to LV filling, stroke volume, and cardiac output

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ECG
Brugada criteria:

 

An algorithm for the diagnosis of VT, most commonly used method7. Overall 98.7% sensitivity and 96.5% specific for VT8. Algorithms for VT tend to misclassify SVT with preexcitation (accessory pathway-mediated) as VT, but preexcitation is an uncommon cause of WCT (6% in one series8).

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Brugada Criteria7
1. Absence of an RS complex in all precordial leads?
- Yes: VT – sensitivity 21%, specificity 100% No: proceed to next question

2. R to S interval > 100 msec?
- Yes: VT – sensitivity 66%, specificity 98% No: proceed to next question

3. AV dissociation*?
- Yes: VT – sensitivity 82%, specificity 98% No: proceed to next question

4. Morphology criteria for VT present both in precordial leads V1-V2 and V6?
- Yes VT – sensitivity 98.7%, specificity 96.5% - No: SVT with aberrancy – sensitivity 96.5%, specificity 98.7% * AV dissociation:

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R to S interval

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Brugada Criteria Algorithm7

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Morphology Criteria9
Features Favoring VT: Features Favoring SVT w/Aberrancy: RBBB pattern:
Triphasic rSR’ in V1 Triphasic rSR’ in V6 R > S in V6

RBBB pattern:
Monophasic R or Biphasic qR, QR, or RS in V1 S > R or QS in V6

LBBB pattern:
Broad R wave or wide RS length ( > 30 msec in V1 or V2) Notched downstroke of S wave in V1 or V2 > 60 msec to nadir of S in V1 or V2 qR or QS pattern in V6

LBBB pattern:
No R in V1 Small narrow R in V2 No slurring of S wave downstroke Monophasic R in V6 Presence of septal Q in I and V6

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Features Favoring VT:

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II. Narrow Complex Tachycardia:
The narrow complex tachycardias, aka “PSVT”:  Sinus Tachycardia (ST)  Inappropriate Sinus Tachycardia (IST)  Sinoatrial Nodal Reentrant Tachycardia (SNRT)  Atrial Tachyardia (AT)  Multifocal Atrial Tachycardia (MAT)*  Atrial Fibrillation (AF)*  Atrial Flutter (AFl)*  Junctional ectopic Tachycardia (JeT)  Junctional Tachycardia (JT)  Permanent Junctional Reciprocating Tachycardia (PJRT)  Nonparoxysmal Junctional Tachycardia (NPJT)  Atrioventricular Nodal Reentrant Tachycardia (AVNRT)  Atrioventricular Reentrant Tachycardia (AVRT) * AF, AFl, and MAT are PSVTs, but commonly classified as separate group * Reentry is the most common cause of narrow complex tachycardia; increased automaticity and triggered activity occur less frequently10.

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Initial Evaluation of Narrow Complex Tachycardias
Rate may be too fast to identify, can try the following to slow the rate:

I. Carotid sinus massage (CSM)  Can slow or even terminate rhythm, as is often the case with AVNRT or AVRT  CSM induces temporary slowing of SA nodal activity and AV nodal conduction by stimulating baroreceptors, which causes increased vagus output and sympathetic withdrawal  Contraindicated if bruit present, prior CVA or TIA, MI within 6 months, h/o VT/VF

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II. Adenosine


   

Can be diagnostic and therapeutic in rhythms that depend on AV node, ie AVNRT, AVRT 6 mg IV followed by 12 mg through peripheral lines, or 1 mg then 3 mg through CVC Transient asystole a “rare side effect” Common side effects include facial flushing (18%), palpitations, CP, hypotension Effects blunted in patients on theophylline, and accentuated in the denervated heart If using in pts suspected of having WPW, have defibrillator ready (not recommended)

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When evaluating a narrow complex tachycardia, assess regularity of rhythm

Irregular:

AF = irregularly irregular, no identifiable P waves, atrial rate 350-600 impulses/min, irregularly irregular ventricular response of 90-170 bpm, or higher if slick AV node. Coarse AF or prominent U waves may give the appearance of P waves MAT = irregularly irregular, at least 3 distinct P wave morphologies, varying P-P, R-R, and PR intervals. Typically seen in elderly pts w/advanced pulmonary disease AFl with block = Mobitz Type I 2nd degree AV block (Wenckebach) can look like AF because it’s irregular, but w/ pattern of grouped beats typical of Wenckebach

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Regular:

Do I see clearly discernible P waves? (best leads to look for P waves are V1 and II) If yes = ST, IST, AT, MAT, AFl, SNRT P Waves Indiscernible: - Most commonly AVNRT, but can also be AF, AVRT, JT11. - JT arises from discrete focus within AV node or His bundle - JT thought to be enhanced automaticity, not reentry - JT seen with AMI, dig toxicity, myocarditis, or post-op due to AV nodal injury - Atrial activity usually retrograde, but AV dissociation can occur

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Atrial Flutter (AFl)
Flutter has an easily identifiable classic appearance: P waves exhibit classic sawtooth pattern  Atrial rate > 250 bpm almost always flutter (cannot measure atrial rate in AF on ECG) - Ventricular rate of exactly 150 should be considered flutter until proven otherwise  Macroreentrant atrial rhythm with reentry circuit involving large area of atrial myocardium, with most common circuit around tricuspid annulus  Atrial tissue between IVC and tricuspid annulus is called the isthmus, and RFA of this region has >90% cure rate  Typical A:V ratio is 2:1, with atrial rate of 300 in typical flutter  Even ratios more common, ie 2:1 or 4:1 - beta blockers and CCBs can cause this  Classic/typical flutter is a counter-clockwise reentrant loop, with negative sawtooth waves in leads II, III, and AVF; most common form of AFl  - Atypical flutter is a clockwise reentrant loop, with positive sawtooth waves in inferior leads, usually slower atrial (and ventricular) rate

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Typical Counter-Clockwise AFl

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Typical Atrial Flutter

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RFA

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Once the rhythm is sufficiently slowed, we must further examine the P waves for characterization of atrial activity.

Key features of atrial activity11:
I. Atrial rate II. P wave morphology – sinus P’s, abnormal, or retrograde III. Correlation with ventricular rate – 1:1? IV. Position of P wave in relation to preceding or following QRS – Short RP vs Long RP

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P Wave Morphology:

Obtain old sinus ECG – if P wave is identical, then ST, IST, SNRT  ST – rate usually 100-180 bpm, can be > 200 in young hearts (remember 220-age) - Normal P wave morphology: axis of 0 to 90 degrees, ie upright in I, II, and AVF - A:V ratio always 1:1  IST - chronic nonparoxysmal sinus tachycardia - Unusual condition, cause unknown, thought to be abnormal autonomic control - Occurs in patients w/out apparent heart disease or physiologic cause for ST  SNRT - Uncommon, < 5% of EP referrals12. - Rate 100-150 - Distinguised from ST by abrupt onset and termination

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Abnormal P Wave Morphology:

If clearly different from sinus P, and RP > PR, likely some form of AT  Can also occur in atypical AVNRT and AVRT w/slowly conducting accessory pathway, aka PJRT  AT: -Regular w/rate 100-250 bpm - Originating in atria outside of sinus node - Often difficult to distinguish from sinus if close to sinus node - Etiology: automatic, triggered, or reentrant - Termination of the tachycardia with a QRS complex more common in AT - Not always 1:1 conduction, especially if atrial rate rapid and AV conduction slow - AT with block – seen with digitalis toxicity

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Retrograde P Wave and Short RP:


 

Most common cause of inverted P waves is improper lead placement True retrograde P waves caused by conduction from AV node toward SA node Typically inverted in II, III, and AVF Retrograde P waves + short RP = Typical AVNRT (90%), AVRT, AT w/1st degree block, and JT Short RP = P wave may appear nearer to the preceding QRS complex (occasionally in or fused w/QRS complex) so that PR interval is greater than RP interval Termination of the tachycardia with a P wave after the last QRS complex most common in AVNRT or AVRT11.

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AVNRT
   

60% of all PSVTs13. Two conduction pathways within the AV node Unidirectional block occurs with PAC Blocked pathway recovers as the impulse conducts slowly down the other pathway and conducts retrograde, creating reentrant loop

Antegrade conduction occurs down the slow pathway and retrograde conduction up the fast pathway…remember “down the slow, up the fast”
Retrograde P waves may be obscured by QRS complex V-A < 70 msec P waves may fall after or at the end of QRS complex, creating a “pseudo R prime” in leads where QRS negative, or “pseudo S wave” in leads where QRS positive

 

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AVRT
AVRT (orthodromic):  Also known as AV reciprocating tachycardia  Antegrade conduction occurs down AV node, resulting in ventricular activation, then retrograde atrial activation occurs later through AV bypass tract  Retrograde P wave follows QRS, usually in ST segment  Classic example is WPW, which is AVRT in opposite direction – down node, up the accessory pathway AVRT (antidromic):  Antegrade conduction occurs through AV bypass tract and retrograde conduction occurs through AV node  This results in a wide complex tachycardia

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Orthodromic AVRT (WPW)

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Orthodromic AVRT (WPW)

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Retrograde P Wave and Long RP:

Long RP = P wave may appear nearer to the following QRS complex, so that

RP interval is greater than the PR interval (AVRT, AT w/out 1st degree block,
PJRT, Atypical AVNRT)

Combination of retrograde P waves and long RP usually caused by atypical/uncommon AVNRT or AVRT w/slowly conducting accessory pathway

Uncommon AVNRT = antegrade conduction down fast pathway and retrograde
conduction through a slow pathway; 10% of AVNRT14.

 

P wave occurs very late in cardiac cycle, near next QRS, hence the long RP PJRT = AVRT w/slowly conducting accessory pathway; antegrade conduction occurs through the AV node, and retrograde conduction occurs through slowly conducting accessory pathway. Also produces long RP

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References:
1. Stewart, RB, Bardy, GH, Greene, HL. Wide complex tachycardia: misdiagnosis and outcome after emergency therapy. Ann Intern Med 1986; 104:766. 2. Akhtar, M, Shenasa, M, Jazayeri, M, et al. Wide complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med 1988; 109:905. 3. Gupta, AK, Thakur, RK. Wide QRS complex tachycardias. Med Clin North Am 2001; 85:245. 4. Miller, JM, Hsia, HH, Rothman, SA, et al. Ventricular tachycardia versus supraventricular tachycardia with aberration: electrocardiographic distinctions. In: Cardiac Electrophysiology From Cell to Bedside. Zipes, DP, Jalife, Jose (Eds), W.B. Saunders, Philadelphia 2000. p.696. 5. Tchou, P, Young, P, Mahmud, R, et al. Useful clinical criteria for the diagnosis of ventricular tachycardia. Am J Med 1988; 84:53. 6. Baerman, JM, Morady, F, DiCarlo, LA Jr, de Buitleir, M. Differentiation of ventricular tachycardia from supraventricular tachycardia with aberration: value of the clinical history. Ann Emerg Med 1987; 16:40. 7. Brugada, P, Brugada, J, Mont, L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649. 8. Miller, JM, Hsia, HH, Rothman, SA, et al. Ventricular tachycardia versus supraventricular tachycardia with aberration: electrocardiographic distinctions. In: Cardiac Electrophysiology From Cell to Bedside. Zipes, DP, Jalife, Jose (Eds), W.B. Saunders, Philadelphia 2000. p.696. 9. Crawford PA, Lin TL. The Washington Manual Cardiology Subspecialty Consult. Lippincott, Williams, and Wilkins, New York, 2004: pp 186-187. 10. Blomstrom-Lundqvist, C, Scheinman, MM, Aliot, EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation 2003; 108:1871. 11. Worldwide Web: Arnsdorf MF, Ganz LI. Approach to narrow QRS complex tachycardias. www.UpToDate.com. 5/24/06 12. Sanders, WE, Sorrentino, RA, Greenfield, RA, et al. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol 1994; 23:926. 13. Trohman, RG. Supraventricular tachycardia: implications for the intensivist. Crit Care Med 2000; 28:N129. 14. Akhtar, M, Jazayeri, MR, Sra, J, et al. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations. Circulation 1993; 88:282. 15. Worldwide Web: Suh, D. VT vs. SVT with aberrancy EKG criteria. http://intmedweb.wfubmc.edu/blurbs/cards/complex.html. 5/24/06

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