1 tachydysrhythmias august 2, 2001 gavin greenfield bryan young

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Tachydysrhythmias

August 2, 2001Gavin Greenfield

Bryan Young

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Outline

• Basic Science• Mechanisms of Tachydysrhythmias

– impulse formation or impulse conduction• Anti-dysrhythmics• Classification• Management of Specific Tachydysrhythmias• Diagnosing Etiology of Wide-Complex

Tachycardia• Practice EKG’s• Revised ACLS Tachycardia Algorithm

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Basic Science - Anatomy

• 3 basic types of myocardial cells• contractile, conductive, pacemaker

– 99% of cardiac muscle cells are contractile

• Innervation– sympathetic via ~T1-T5

• neurotransmitter? receptor?

– parasympathetic via vagus nerve• neurotransmitter?

– both innervate cells of both the contractile and conductive systems

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Basic Science - Electrophysiology

• Depolarization– common to contractile and conductive cells

• Action Potential

• Resting Membrane Potential

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Basic Science - ElectrophysiologyResting Membrane Potential

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Basic Science - Depolarization

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Basic Science - Depolarization

• Differences between contractile cells and those involved in conduction

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Basic Science – Effect of Autonomic Nervous System on

Depolarization• Sympathetic stimulation increases slope of

phase 4 depolarization

• Parasympathetic stimulation decreases slope of phase 4 depolarization– parasympathetic stimulation also

hyperpolarizes membrane (potential starts from lower value)

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Basic Science – Sequence of Excitation

• SA node is dominant pacemaker – why?• Blood supply to SA node?• Pathway of action potential from SA node

to AV node?• Blood supply to AV node?• AV node to bundle of His to R and L BB’s

to Purkinje fibers• Purkinje fibers rapidly distribute impulse to

contractile cells in ventricles

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Basic Science – Refractory Period

• Refractory Period definition

• Cardiac muscle cells have long refractory period (this prevents tetanic contractions and therefore allows filling)

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Mechanisms for Tachydysrhythmia Formation

• Altered automaticity increased automaticity in normal (enhanced automaticity) or ectopic (abnormal automaticity) site

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• Reentry in normal or accessory pathway

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• Triggered Dysrhythmias

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Pharmacology of Anti-dysrhythmics

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• 4 Broad Classes– based on effect on action potential and impulse

conduction

• Classification system ignores multiple overlapping properties of drugs– agents classified according to major effect

• Class I – sodium channel blockers• Class II – beta-adrenergic blockers• Class III – antifibrillatory agents• Class IV – calcium channel blockers

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• Class I (Sodium Channel Blockers)– Which part of action potential is therefore

inhibited?

• phase 0 is inhibited resulting in slowed depolarization and therefore slowed conduction and membrane stabilization (therefore prominent anti-ectopic effects)– varying effects on repolarization

• 3 subclasses 1A, 1B, 1C

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Pharmacology of Anti-dysrhythmicsClass I – sodium channel blockers

• Class 1A– Procainamide– Quinidine– Disopyramide

• Specific Effects– moderately slow depolarization and conduction– prolong repolarization and action potential duration– clinically results in slowed conduction through atria,

AV node, and His-Purkinje system– also decreases conduction in accessory pathways

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• Class 1B– lidocaine– phenytoin– tocainide, mexiletine, moricizine, aprindine

• Specific Effects– minimally slow depolarization and conduction– shorten repolarization and action potential

duration (1A and 1C prolong)

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• Class 1C– Propafenone (also some 1A properties)– Flecainide, Encainide, Lorcainide

• Specific Effects– profoundly slow depolarization and

conduction– prolong repolarization and action potential

duration

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Pharmacology of Anti-dysrhythmicsClass II – Beta adrenergic blockers• Metoprolol, Esmolol, Acebutolol, Nadolol,

Propranolol

• Specific Effects (think of NE and Beta 1 actions on depolarization and contractility)– slow SA node impulse formation, slow AV

conduction, prolong action potential and can depress conduction in ischemic tissue

– depress myocardial contractility

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Pharmacology of Anti-dysrhythmicsClass III – antifibrillatory agents

• Amiodarone• Bretylium• Sotalol (shares activity with Class II)• Ibutilide (shares activity with Class II)

• Specific Effects– prolong action potential duration and

refractory period duration thus exhibiting antifibrillatory properties

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Pharmacology of Anti-dysrhythmicsClass IV – Calcium (slow) channel

blockers• Diltiazem, Verapamil

• Specific Effects– block calcium entry to cells thus causing

depression of anterograde conduction through AV node and suppression of other calcium-dependent dysrhythmias

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Pharmacology of Anti-dysrhythmicsMiscellaneous

• Adenosine– naturally occurring purine nucleoside– causes concentration dependent slowing of

AV conduction and slowing of both anterograde and retrograde paths of a reentrant circuit

– at antidysrhythmic doses has peripheral vasodilatory properties

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Pharmacology of Anti-dysrhythmicsMiscellaneous

• Digoxin– positive inotrope– variable electrophysiological effects on

myocardial cells – can divide into excitant and depressant (therapeutic effects are result of depressant actions)

– Excitant – increase in altered automatic and triggered ectopic impulses

– Depressant – depresses conduction and lengthens refractoriness in AV node

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All anti-dysrhythmics are pro-arrhythmics

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Amiodarone

• Effects– complex drug with effects on sodium,

potassium, and calcium channels– alpha adrenergic and beta adrenergic

blocking properties – prolongs action potential duration and

refractory period– slows automaticity in pacemaker cells– slows conduction in AV node– causes smooth muscle relaxation

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Amiodarone – “ARREST” Trial

• Kudenchuk et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation, NEJM 341(12), 871-8, September 16, 1999.

• prospective trial of VF/pulseless Vtach after first 3 shocks, intubation and 1 mg Epi

• Amiodarone vs placebo followed by routine antiarrhythmic drugs

• statistically significant increase in survival to hospital admission in amiodarone group

• trial lacked statistical power to detect differences in survival to hospital discharge, which differed only slightly between the two groups

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Tachydysrhythmia Classification

• Several ways to classify tachydysrhythmias:– mechanism of formation– anatomic– EKG appearance– stable vs. unstable

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Tachydysrhythmia ClassificationDecision Point 1

• Stable vs. Unstable: How do we differentiate?• unstable condition must be related to

tachycardia• chest pain suggestive of myocardial ischemia• shortness of breath / pulmonary edema /

congestive heart failure• shock / decreased LOC / hypotension• If unstable it doesn’t matter what the rhythm is –

just sedate and cardiovert

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Specific Dysrhythmias

• Narrow QRS (supraventricular tachys)– Sinus tachycardia– Ectopic atrial tachycardia– Multifocal atrial tachycardia– Atrial fibrillation– Atrial flutter– AV nodal reentrant tachycardia– Atrioventricular reentrant tachycardia– Junctional tachycardia

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Specific Dysrhtyhmias

• Wide QRS– ventricular tachycardia– ventricular fibrillation– any supraventricular tachycardia with aberrant

conduction

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Narrow-Complex TachycardiasSinus Tachycardia

• from acceleration of SA Node discharge rate• Atrial rate usually between 100 and 160• sinus tachycardia is a response to: 1.

physiologic stress (exertion, anxiety, etc.) 2. pharmacologic influence (caffeine, nicotine, alcohol, sympathomimetics) 3. pathologic (fever, anemia, hypoxia, hypotension, etc.)

• Treat underlying condition

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Narrow-Complex TachycardiasAtrial Tachycardia

• from any nonsinus focus above AV Node

• each QRS preceded by P’

• if no old EKG difficult to differentiate from sinus tachycardia

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Narrow-Complex TachycardiasMultifocal atrial tachyardia

• subset of atrial tachycardia aka wandering pacemaker

• irregular rhythm, often confused with afib

• at least three foci of impulse formation, therefore 3 distinctly different P waves

• often associated with pulmonary disease and hypoxemia

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Treatment of Atrial and Multifocal Atrial Tachycardia

• causes:• include electrolyte and acid-base disturbances,

drug toxicity, fever, hypoxemia• MFAT classically associated with pulmonary

disease and hypoxemia• Treat underlying disorder• if pt symptomatic can treat with Beta blocker or

Calcium channel blocker or Amiodarone• Magnesium second line agent• Procainamide and digoxin can also be used

– specific antiarrhythmic therapy is rarely indicated

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Narrow Complex TachycardiasSVT

• regular rapid rhythm that arises from either reentry or ectopic pacemaker in area above bifurcation of bundle of His

• reentrant variety often presents as PSVT

• 60% have reentry within AV node

• 20% have reentry involving bypass tract

• remainder have reentry in other sites

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• Reentry in normal or accessory pathway

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SVT

• 2 types of reentry SVT• AV Nodal Reentrant Tachycardia (AVNRT)

– dual AV nodal pathways– initiated with ectopic atrial impulse

encountering AV node during partial refractory period

• 2nd type of reentry is Atrioventricular reentry (AVRT)– What is AVRT dependent upon?

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SVTAtrioventricular reentrant

tachycardia (AVRT)• seen in patients with bypass tracts

• What is classic example?

• second connection (other than AV node) present between atria and ventricles

• like AVNRT, AVRT usually initiated by ectopic extrasystole

• 2 types of conduction

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SVTWPW

• 2 types of conduction• orthodromic conduction (85% of WPW)

– impulse conducted anterogradely down AV node and retrogradely up bypass tract

– produces narrow QRS

• antidromic conduction (15% of WPW)– impulse conducted anterogradely down

accessory tract and up AV node– wide QRS – difficult to differentiate from vtach

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SVT

• etiology of reentrant SVT– can occur in normal heart, or in association

with rheumatic heart disease, acute pericarditis, MI, mitral valve prolapse, or one of the pre-excitation syndromes (WPW)

• with compromised heart can get– anginal chest pain, dyspnea, pulmonary

edema from decreased diastolic filling

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SVT Treatment

• can treat by impeding conduction through one limb of reentry circuit– sustained reentry then impossible and sinus

node can take over

• increase vagal tone – “vagal maneuvers”– carotid sinus massage (Munro NC, McIntosh S, Lawson J, et

al: Incidence of complications after carotid sinus massage in older patients with

syncope. J Am Geriatr Soc 1994;42:1248-1251 ) – Valsalva – most effective vagal maneuver– facial immersion in cold water

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SVT Treatment• Pharmacologic• Hood MA, Smith WM: Adenosine versus verapamil in the treatment of supraventricular tachycardia: A

randomized double-crossover trial. Am Heart J 1992;123:1543-1549 • Taylor DM - Am J Emerg Med - 1999 Mar; 17(2): 214-6

• Brady WJ Jr. DeBehnke DJ. Wickman LL. Lindbeck G. Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil. [see comments]. [Journal Article] Academic Emergency Medicine. 3(6):574-85, 1996 Jun.

– Adenosine• MOA?• dose?• side effects?

– Verapamil• 0.075 to 0.15 mg/kg (3-10 mg) IV over 15-60 sec• repeat dose in 30 min if necessary• associated with hypotension

– Diltiazem, Beta blockers, digoxin – Consider procainamide, amiodarone, sotalol (2000 ACLS)

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Atrial Flutter

• Definition (Rosen)– regular atrial depolarization rate of 250 to 350 bpm;

classically 300– distinct EKG manifestations of abnormal atrial

depolarization in a sawtooth appearance– common association with a 2:1 block (ventricular rate

of 150 or 4:1 block)– can see irregular rhythm with variable conduction

(sometimes profound bradycardia)

• pathophysiology thought to be reentry and or abnormal automaticity

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Atrial Flutter

• often associated with underlying heart disease– IHD, CHF, valvular

dysfunction, PE– metabolic

derangements

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Atrial Flutter - Treatment

• Of course, cardioversion if unstable– low energy required – start at 25-50 J

• treat underlying cause (if known)• Pharmacologic (Rate Control)

– ventricular rate control with calcium channel blocker (Diltiazem or Verapamil) or beta blocker

– if preexisting CHF (EF < 40%) consider diltiazem, digoxin, amiodarone (ACLS 2000)

– can think of using adenosine to unmask flutter waves if diagnosis uncertain

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Atrial Flutter - Treatment

• Pharmacologic (Conversion)– Class 1A (procainamide), Class 1C

(propafenone, flecainide), Class III (amiodarone, ibutilide) – ACLS 2000

– consider amiodarone if CHF (EF < 40%) (ACLS 2000)

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Atrial Fibrillation• Causes (heart, PE, metabolic)

– IHD, acute MI– valvular heart disease (esp. mitral)– hypertensive heart disease– pericarditis– myocardial contusion– cardiomyopathy– cardiac surgery– congestive heart failure– sick sinus syndrome– acute ethanol intoxication (“holiday heart”)– catecholamine excess– hyperthyroidism– accessory pathway (WPW)– pulmonary embolism– idiopathic

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Atrial Fibrillation

• completely irregular rhythm because of irregular ventricular response

• loss of coordinated atrial activity and potentially rapid ventricular response can lead to decreased cardiac output (reduced diastolic filling)

• paroxysmal or chronic• fibrillatory waves best seen inferiorly and V1• multiple atrial microreentry circuits results in

“atrial rate” of 300-600

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Atrial Fibrillation – Rate Control

• rates of 120 and less usually do not require emergent treatment

• if unstable sedate and cardiovert (start at 50-100J)

• Calcium channel blockers• Beta blockers

– especially good for hyperthyroid related afib

• Consider Digoxin and Amiodarone in compromised LV (EF<40%)

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• Roy D. Talajic M. Dorian P. Connolly S. Eisenberg MJ. Green M. Kus T. Lambert J. Dubuc M. Gagne P. Nattel S. Thibault B. Amiodarone to prevent recurrence of atrial fibrillation. Canadian Trial of Atrial Fibrillation Investigators. [see comments]. [Clinical Trial. Journal Article. Multicenter Study. Randomized Controlled Trial] New England Journal of Medicine. 342(13):913-20, 2000 Mar 30.

– amiodarone vs. sotalol and propafenone for prevention of recurrence– pt’s were electrically cardioverted if no spontaneous cardioversion by 3 weeks– 35% of pt’s treated with amiodarone had recurrence, 63% treated with sotalol or

propafenone had recurrence– did not specifically look at initial conversion rates – only avoidance of recurrence

• Joseph AP. Ward MR. A prospective, randomized controlled trial comparing the efficacy and safety of sotalol, amiodarone, and digoxin for the reversion of new-onset atrial fibrillation. [Clinical Trial. Journal Article. Randomized Controlled Trial] Annals of Emergency Medicine. 36(1):1-9, 2000 Jul.

– AFib < 24 h duration– sotalol vs amiodarone vs digoxin– time to reversion 13 h with sotalol, 18 h with amiodarone, 26.9 h with digoxin– concluded that sotalol and amiodarone both better than digoxin– in pt’s who were still in atrial fibrillation sotalol provided the best ventricular rate control

Atrial FibrillationPharmacologic Conversion Studies

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• Vardas PE. Kochiadakis GE. Igoumenidis NE. Tsatsakis AM. Simantirakis EN. Chlouverakis GI. Amiodarone as a first-choice drug for restoring sinus rhythm in patients with atrial fibrillation: a randomized, controlled study. [see comments]. [Clinical Trial. Journal Article. Randomized Controlled Trial] Chest. 117(6):1538-45, 2000 Jun.

– amiodarone vs. placebo– no regard to duration of afib– 80% of amiodarone group and 40% of placebo group converted by 30 days

• Blanc JJ. Voinov C. Maarek M. Comparison of oral loading dose of propafenone and amiodarone for converting recent-onset atrial fibrillation. PARSIFAL Study Group. [see comments]. [Clinical Trial. Journal Article. Multicenter Study. Randomized Controlled Trial] American Journal of Cardiology. 84(9):1029-32, 1999 Nov 1.

– oral amiodarone vs. oral propafenone for conversion in Afib < 2 weeks duration– median time to conversion 2.4 h (propafenone) and 6.9 h (amiodarone)– after 24 and 48 h same proportion of pt’s recovered sinus rhythm (56 and 47%)

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• . Kochiadakis GE. Igoumenidis NE. Simantirakis EN. Marketou ME. Parthenakis FI. Mezilis NE. Vardas PE. Intravenous propafenone versus intravenous amiodarone in the management of atrial fibrillation of recent onset: a placebo-controlled study. [Clinical Trial. Journal Article. Randomized Controlled Trial] Pacing & Clinical Electrophysiology. 21(11 Pt 2):2475-9, 1998 Nov.

– propafenone vs. amiodarone vs. placebo in recent onset Afib (<48h duration)– 78% conversion in propafenone, 83% conversion in amiodarone, 55%

conversion in placebo– mean time to conversion 2+/- 3 h for propafenone, 7+/- 5 h for amiodarone– conclusion was both drugs equally effective and safe for conversion but

propafenone faster• Mattioli AV. Lucchi GR. Vivoli D. Mattioli G. Propafenone versus

procainamide for conversion of atrial fibrillation to sinus rhythm. [Clinical Trial. Controlled Clinical Trial. Journal Article. Randomized Controlled Trial] Clinical Cardiology. 21(10):763-6, 1998 Oct.

– procainamide vs. propafenone– procainamide (69.5%) more effective than propafenone (48.7%) for conversion to

sinus rhythm

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Atrial Fibrillation 2000 ACLS Guidelines

• Duration <48 h• DC cardioversion• amiodarone, procainamide, propafenone, ibutilide, flecainide

(all class IIa)

• Duration > 48 h• no DC cardioversion• use antiarrhythmics with extreme caution• delayed cardioversion – anticoagulate x 3 weeks, then

cardiovert, and anticoagulate x 4 more weeks OR early cardioversion – IV heparin, TEE to exclude clot, then cardiovert and anticoagulate x 4 more weeks (journal club)

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Carlson, Cardiology in Review, 9(2), 2001

• Reviewed numerous trials regarding afib and summarized their conclusions:– biphasic waveform shocks more effective than

monophasic waveform shocks for conversion– amiodarone is more effective than either

propafenone or sotalol for maintaining SR in pt’s with Afib

– in a trial of several drugs, combination of atenolol plus digoxin was most effective for control of ventricular rates

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Atrial Fibrillation

• Ongoing trial called AFFIRM trial

• looking at mortality with allowing afib to continue while controlling rate and using anti-thrombotic therapy vs restoring sinus rhythm with antiarrhythmic drugs

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Falk, NEJM, April 5, 2001excellent review of atrial fibrillation

• spontaneous conversion to sinus rhythm within 24 h after onset of new afib is common (about 2/3rds). Once duration exceeds 24 h the likelihood of conversion decreases

• if onset of afib precisely known then consider rate controlling only for 24 hours

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Specific Dysrhythmias

• Narrow QRS (supraventricular tachys)– Sinus tachycardia– Ectopic atrial tachycardia– Multifocal atrial tachycardia– Atrial fibrillation– Atrial flutter– AV nodal reentrant tachycardia– Atrioventricular reentrant tachycardia– Junctional tachycardia

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Preexcitation and Accessory Pathway Syndromes

• preexcitation defined as depolarization of ventricle earlier than would occur by conduction of impulse through AV node– implies existence of accessory pathway

(normally AV node only connection)– WPW most common accessory pathway

syndrome

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Preexcitation and Accessory Pathway Syndromes

• Any tachycardia at rate of 200 bpm or greater should raise suspicion for an accessory pathway syndrome as that is near limit of AV conduction

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SVTWPW

• 2 types of conduction• orthodromic conduction (85% of WPW)

– impulse conducted anterogradely down AV node and retrogradely up bypass tract

– produces narrow QRS

• antidromic conduction (15% of WPW)– impulse conducted anterogradely down

accessory tract and up AV node– wide QRS – difficult to differentiate from vtach

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Ventricular Tachydysrhythmias

• Ventricular Tachycardia– monomorphic ventricular tachycardia

• morphologically consistent QRS complexes• usually regular rhythm• rate usually 150-200• can occur in presence or absence of IHD

– polymorphic ventricular tachycardia• QRS complexes that vary in structure or duration• associated with more severe underlying disease than

monomorphic vtach• Torsades de pointes is a specific form

– for treatment an important principal to remember is to correct any underlying causes

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Stable Monomorphic Ventricular Tachycardia

• Treatment (ACLS 2000)

• Normal Cardiac Function– procainamide, sotalol– amiodarone, lidocaine

• EF < 40% or evidence CHF– amiodarone or lidocaine then synchronized

cardioversion

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Stable Polymorphic Ventricular Tachycardia

• ACLS 2000• Classified based on QT interval• Normal baseline QT (not torsades)

– treat ischemia– correct electrolytes– consider Beta blockers or lidocaine or amiodarone or

procainamide or sotalol– if EF < 40% or evidence CHF then amiodarone or

lidocaine followed by synchronized cardioversion

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Stable Polymorphic Ventricular Tachycardia

• ACLS 2000• prolonged baseline QT interval (suggests

torsades)– correct abnormal electrolytes– consider magnesium, lidocaine, isoproterenol,

phenytoin, overdrive pacing– 1A and 1C contraindicated because prolong

repolarization– sustained or unstable torsades - cardiovert

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Torsades de pointes

• Must meet three criteria to be called torsades

• ventricular rate greater than 200• QRS displays undulating axis with polarity

of complexes appearing to shift about baseline

• occurrences are often in short episodes of less than 90 seconds, although sustained runs can be seen

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Torsades de pointes

• often occurs in setting of prolonged QT interval during sinus rhythm (repolarization abnormality)

• repolarization abnormality (prolonged QT) can be congenital or acquired

• acquired QT prolongation often result of drug therapy, electrolyte disturbances (hypoK+, hypoMg++)

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Torsades de pointes

• 2 types

• Pause dependent (acquired)

• Adrenergic dependent (acquired or congenital)

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Torsades de pointes

• Pause dependent (acquired)– drug induced– electrolyte abnormalities– severe bradycardia or AV block– myocardial ischemia– hypothyroid– contrast injection– CVA (especially intraparenchymal)

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Torsades de pointes

• Adrenergic dependent– acquired

• subarachnoid hemorrhage• autonomic surgery (radical neck dissection, carotid

endarterectomy, truncal vagotomy)

– congenital• Jervell and Lange-Nielsen syndrome (deafness, autosomal

recessive)• Romano-Ward syndrome (normal hearing, autosomal

dominant)• sporadic (normal hearing, no family tendency)• mitral valve prolapse

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Passman, Medical Clinics of North America, 85(2), March 2001

Treatment of PMVT associated with acquired Long QT (Torsades)

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Approach to EKG Dysrhythmia interpretation

• rate: ventricular rate fast (>100), slow (<60) or normal• rhythm: regular or irregular or regular with occasional

irregularities– use calipers for subtle irregularities– long rhythm strips (2 min) sometimes required

• QRS width: prolonged (>0.12 sec), borderline (0.09-0.12 sec), or normal

• P wave presence and relationship to QRS complexes– may require mapping of P-waves with calipers to detect those

falling within QRS complex or T wave– can increase paper speed to better define p – QRS relationship

• examine multiple leads• compare with previous tracing

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Differential Diagnosis of Wide Complex Tachycardia

• ventricular tachycardia vs. supraventricular source (with aberrancy or accessory pathway)

• Look at history, physical examination and EKG tracing

• Morady et al. have shown that stable pt’s are overdiagnosed as SVT with aberrancy, with sometimes lethal consequences

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Differential Diagnosis of Wide Complex Tachycardia

• Wellens criteria– Wellens HJJ, Bar F, Lie KI: The value of the

electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex, Am J Med 64:27, 1978.

– Wellens HJJ: The wide QRS tachycardia (editorial), Ann Intern Med 104:879, 1986.

– look at history, physical examination, EKG

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Ventricular tachycardia

Supraventricular tachycardia plus

aberrancy

History Age 50 or older Age 35 or less

History of myocardial infarction, congestive heart failure, CABG, or ASHD

None

Mitral valve prolapse Mitral valve prolapse (especially in Wolff-Parkinson-White syndrome)

Previous history of ventricular tachycardia

Previous history of supraventricular tachycardia

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Ventricular tachycardia Supraventricular tachycardia plus aberrancy

Physical examination Cannon A waves Absent

Variation in arterial pulse Absence of variability

Variable first heart sound Absence of variability

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Ventricular tachycardia Supraventricular tachycardia plus aberrancy

EKG Fusion beats None

AV dissociation Preceding P waves with QRS complexes

QRS >0.14 sec QRS usually <0.14 sec

Extreme LAD (<-30 degrees)

Axis normal or slightly abnormal

No response to vagal maneuvers

Slow or terminate with vagal maneuvers

Specific QRS patterns V1 : R, qR, or RS V1: rsR`

V6 : S, rS, or qR V6: qRs

Identical to previous ventricular tachycardia tracing

Identical to previous supraventricular tachycardia tracing

Concordance of positivity or negativity

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Brugada Criteria

• 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 83:1649, 1991. Rhythm must be regular to apply criteria– Absence of any RS complexes in the chest leads – RS duration (measured from beginning of R to

deepest part of S wave) >0.1 sec – AV dissociation (variation in first heart sound or in

SBP beat to beat, or cannon jugular waves)• also EKG evidence of AV dissociation

– Specific ventricular tachycardia morphologic criteria

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The morphology associated with the fourth criterion in the Brugada system in patients with a right bundle branch-

appearing complex.

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The morphology associated with the fourth criterion in the Brugada system in patients with a left bundle branch-

appearing complex.

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Brugada Criteria

• Only when none of the four criteria is met do we diagnose a supraventricular etiology

• as soon as answer yes vtach diagnosed

• original study found sensitivity 98.7% and specificity 96.5%

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Bottom Line

• assume any new onset symptomatic wide-complex tachycardia is vtach until proven otherwise (but can potentially prove otherwise by history, physical examination and EKG)

• can not use blood pressure and LOC (stable vs. unstable) to differentiate

• irregularity suggests afib with aberrancy• When in doubt consider Procainamide because

it is indicated for both (except 1A and 1C contraindicated in Torsades because prolong repolarization)

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EKG Rhythm Diagnosis

• Rate• Rhythm regular or irregular

– irregular is atrial fibrillation, multifocal atrial tachycardia, any supraventricular rhythm with variable conduction, occasionally ventricular tachycardia

• P wave presence and relation to QRS– if normal p’s prior to each QRS and regular rhythm then have

sinus tach, atrial flutter, single focus ectopic atrial tach

• QRS width• Can’t see p wave?

– look in multiple leads– can try long rhythm strip– can increase paper speed to draw out complexes

1 tachydysrhythmias august 2, 2001 gavin greenfield bryan young

Documents

conduction slide

membrane potential slide

filling slide

c slide

accessory pathway slide

contractile cells

lower value slide

basic science anatomy