Tachydysrhymias Stefan Da Silva Oct 19 th 2006 Special Guest: Dr. Phil Ukrainetz With a little help from Drs. R. Hall and D. Peterson.

TachydysrhymiasTachydysrhymias

Stefan Da SilvaStefan Da SilvaOct 19Oct 19thth 2006 2006

Special Guest: Dr. Phil UkrainetzSpecial Guest: Dr. Phil UkrainetzWith a little help from Drs. R. Hall and With a little help from Drs. R. Hall and

D. PetersonD. Peterson

TachydysrhythmiasTachydysrhythmias

Dysrhythmia: any abnormality in Dysrhythmia: any abnormality in cardiac rhythmcardiac rhythm

AnatomyAnatomy SA nodeSA node AV nodeAV node Bundle BranchesBundle Branches



Cardiac Electrophysiology (the very Cardiac Electrophysiology (the very basics!)basics!) Na/K pump Na/K pump

3 Na OUT3 Na OUT 2 K IN2 K IN

This generates approx 10 mV potential across This generates approx 10 mV potential across membranemembrane

The flow of K down the concentration gradient The flow of K down the concentration gradient toward the ECF generates another 80 mVtoward the ECF generates another 80 mV

Ca is also exchanged for Na along membrane via Ca is also exchanged for Na along membrane via osmotic gradientosmotic gradient

= 90 mV membrane resting potential= 90 mV membrane resting potential




Mechanisms for DysrhythmiasMechanisms for Dysrhythmias Altered AutomaticityAltered Automaticity Re-entryRe-entry Triggered MechanismsTriggered Mechanisms

TachydysrhythmiasTachydysrhythmias Altered AutomaticityAltered Automaticity

Impulse relatedImpulse related Can occur in multiple settings (ischemia, Can occur in multiple settings (ischemia,

electrolyte abnormalities, drugs…)electrolyte abnormalities, drugs…) Can be a result of spontaneous phase 4 Can be a result of spontaneous phase 4

depolarization in “non-pacemaker” cells (abnormal depolarization in “non-pacemaker” cells (abnormal automaticity)automaticity)

Eg. VT after MI Eg. VT after MI Increase in the slope of depolarization causing it Increase in the slope of depolarization causing it

to be more positive/closer to threshold (enhanced to be more positive/closer to threshold (enhanced automaticity)automaticity)

Eg. Idioventricular rhythm after MIEg. Idioventricular rhythm after MI Enhanced automaticity as a result of catecholamine Enhanced automaticity as a result of catecholamine

increase stimulating non-SA nodal pacemakers.increase stimulating non-SA nodal pacemakers.


Re-entryRe-entry Conduction relatedConduction related Most common cause of narrow complex Most common cause of narrow complex

rhythms (50% - 80%)rhythms (50% - 80%) Need 3 conditions for re-entryNeed 3 conditions for re-entry

1) Pathway 1) Pathway 2 paths available 2 paths available 2) Unequal responsiveness between routes2) Unequal responsiveness between routes 3) Decrease in conduction of one route3) Decrease in conduction of one route


What happens???What happens??? Dysfunction at the junctionDysfunction at the junction

Impulse finds one route “dysfunctional” (ie. Impulse finds one route “dysfunctional” (ie. in refractory phase) therefore travels down in refractory phase) therefore travels down alternate route and circles back up towards alternate route and circles back up towards initial route (retrograde) since it has initial route (retrograde) since it has recovered from refractory period.recovered from refractory period.

Can result in narrow complex tachycardiaCan result in narrow complex tachycardia

TachydysrhythmiasTachydysrhythmias TriggeredTriggered

Result of “afterdepolarization” Result of “afterdepolarization” fluctuations in fluctuations in membrane potential that occur as the resting membrane potential that occur as the resting potential is approached which may precipitate potential is approached which may precipitate another depolarizationanother depolarization

Dependant on heart rate for propagationDependant on heart rate for propagation Can be either early or late afterdepolarizations.Can be either early or late afterdepolarizations. Late: enhanced by faster heart rates. eg. Late: enhanced by faster heart rates. eg.

Intracellular Ca overload in reperfusion therapy Intracellular Ca overload in reperfusion therapy post MI can cause dysrhythmias such as VT, post MI can cause dysrhythmias such as VT, bigeminy, junctional rhythmsbigeminy, junctional rhythms

Early: enhanced by slower heart rates. eg. Early: enhanced by slower heart rates. eg. Torsades de pointes Torsades de pointes

Triggered ActivityTriggered Activity(early afterdepolarizations)(early afterdepolarizations)

Early afterdepolar-izations occur during either phase 2 or phase 3 of the action potential, and are seen most commonly in QT prolongation.

Triggered ActivityTriggered Activity(late afterdepolarizations)(late afterdepolarizations)

Late afterdepolar-izations occur shortly after completion of repolarization, and are seen most commonly in digitalis intoxication and high catecholamine states.


Antidysrhythmic DrugsAntidysrhythmic Drugs Class IClass I

Na (fast) channel blockersNa (fast) channel blockers ““Membrane stabilizing”Membrane stabilizing” Anti-ectopic effectsAnti-ectopic effects

IA: slows deplolarization and conduction. IA: slows deplolarization and conduction. Prolong repolarization and AP duration Prolong repolarization and AP duration

Eg. Procainamide: dosage Eg. Procainamide: dosage 20 – 30 mg/min 20 – 30 mg/min until termination of dysrhythmia, decrease in until termination of dysrhythmia, decrease in BP, widening QRS greater than 50% of initial BP, widening QRS greater than 50% of initial width or total dose of 18 – 20 mg/kg width or total dose of 18 – 20 mg/kg adminstered (can be given up to 50 mg/min in adminstered (can be given up to 50 mg/min in “urgent” situations..)“urgent” situations..)

Maintenance: 1 – 4 mg/minMaintenance: 1 – 4 mg/min Can be given orally as outpt.Can be given orally as outpt.


IB: slows depolarization and conduction. IB: slows depolarization and conduction. Shorten repolarization and action potential Shorten repolarization and action potential durationduration

Eg. Lidocaine: DosingEg. Lidocaine: Dosing 1.0 - 1.5mg/kg IV single dose (if refractory can 1.0 - 1.5mg/kg IV single dose (if refractory can

repeat dose 0.5 – 0.75 mg/kg IV q 5 – 10mins…max repeat dose 0.5 – 0.75 mg/kg IV q 5 – 10mins…max dose 3 mg/kg)dose 3 mg/kg)

IC: markedly slows depolarization and IC: markedly slows depolarization and conduction. Prolongs repolarization and conduction. Prolongs repolarization and action potential durationaction potential duration

Eg. PropafenoneEg. Propafenone 1 – 2 mg/kg at 10mg/min….infuse slowly1 – 2 mg/kg at 10mg/min….infuse slowly

TachydysrhythmiasTachydysrhythmias Class IIClass II

B-Blockers (all the “ol’s”…propanolol, esmolol, B-Blockers (all the “ol’s”…propanolol, esmolol, metoprolol)metoprolol)

Slow SA node rate and AV conductionSlow SA node rate and AV conduction Prolong action potentialProlong action potential Depress conduction in ischemic myocardial tissuesDepress conduction in ischemic myocardial tissues

Class IIIClass III Prolong action potential and refractory periodProlong action potential and refractory period Exhibit antifibrillartory effectsExhibit antifibrillartory effects Eg. AmiodaroneEg. Amiodarone

Dosing: Dosing: Arrest: 300mg IV push then 150 mg IV in 3 to 5 mins..max Arrest: 300mg IV push then 150 mg IV in 3 to 5 mins..max

dose in 24 hrs is 2.2g dose in 24 hrs is 2.2g Arrhythmias: 150 mg IV over 1Arrhythmias: 150 mg IV over 1stst 10 minutes can repeat q 10 minutes can repeat q

10 min as needed to max dose.10 min as needed to max dose.


Class IVClass IV Slow Ca channel blockersSlow Ca channel blockers Depress anterograde conduction Depress anterograde conduction

through AV node.through AV node. Eg. Diltiazem Eg. Diltiazem

Dosing: 15 – 20 mg IV over 2 minutes, can Dosing: 15 – 20 mg IV over 2 minutes, can repeat at 20 – 25 mg IV after 15 minutesrepeat at 20 – 25 mg IV after 15 minutes

Can give Calcium prior to decrease Can give Calcium prior to decrease hypotensive effectshypotensive effects


ApproachApproach ABC’sABC’s Stable vs non-stableStable vs non-stable ECGECG

Wide vs Narrow!!!Wide vs Narrow!!! Regular vs IrregularRegular vs Irregular P waves vs No P wavesP waves vs No P waves

Old Chart (old ECG’s extremely helpful)Old Chart (old ECG’s extremely helpful)

TachydysrhythmiasTachydysrhythmias What do you want to know?What do you want to know?

Stable or not stableStable or not stable Stable…now what?Stable…now what?

Have time to do focussed hx and physicalHave time to do focussed hx and physical Hx: Hx:

timing, palpitations, dizziness, chest pain, SOB, timing, palpitations, dizziness, chest pain, SOB, syncope etcsyncope etc

Previous hx of similarPrevious hx of similar MedicationsMedications

PhysicalPhysical Evidence of end-organ perfusion/alteration in Evidence of end-organ perfusion/alteration in

cognitioncognition Regular cardio-pulmonary exam.Regular cardio-pulmonary exam.

ECGECG InterventionsInterventions

Case #1Case #1 76 yr old male presenting with 1 day hx 76 yr old male presenting with 1 day hx

of heart “racing” and mild breathlessof heart “racing” and mild breathless PMHx: “some heart problems”PMHx: “some heart problems” Meds: “…half a blue pill for BP and Meds: “…half a blue pill for BP and

water pill or something like that…”water pill or something like that…” Vitals: fluctuating HR 120 – 150, BP Vitals: fluctuating HR 120 – 150, BP

160/96, Sat 96% RA, 36.5 temp160/96, Sat 96% RA, 36.5 temp



CASE #1CASE #1

TachydysrhythmiasTachydysrhythmias Atrial FibrillationAtrial Fibrillation

““chaos”chaos” Irregularly irregularIrregularly irregular No distinct “P” wavesNo distinct “P” waves Narrow Complex Narrow Complex

Ashman Phenomenon: isolated/repeated aberrant Ashman Phenomenon: isolated/repeated aberrant ventricular conduction in RBBB patternventricular conduction in RBBB pattern

Atrial rates of ~300 bpmAtrial rates of ~300 bpm Ventricular rates ~ 150 – 200Ventricular rates ~ 150 – 200 Can be dangerous in patients with LV dysfunction as Can be dangerous in patients with LV dysfunction as

high likelihood of going into heart failure if in Afib high likelihood of going into heart failure if in Afib If > 200 bpm beware of accessory pathway and If > 200 bpm beware of accessory pathway and

predisposition to Vfibpredisposition to Vfib

TachydysrhythmiasTachydysrhythmias Causes: IHD, pericarditis, thyroid dysfunction, Causes: IHD, pericarditis, thyroid dysfunction,

cardiomyopathy, PE, CHFcardiomyopathy, PE, CHF Tx: Tx:

Stable vs unstableStable vs unstable Immediate cardioversion if unstableImmediate cardioversion if unstable

Rate controlRate control Preserved vs unpreserved ventricular functionPreserved vs unpreserved ventricular function Ca++/B-blockersCa++/B-blockers If in doubt Diltiazem can be used for both normal and impaired LV If in doubt Diltiazem can be used for both normal and impaired LV

function (ACLS)function (ACLS) Rhythm controlRhythm control

Duration Duration Chemical vs ElectricalChemical vs Electrical

AmiodaroneAmiodarone AnticoagulationAnticoagulation

Anticoag clinicsAnticoag clinics Afib clinic here in CalgaryAfib clinic here in Calgary Don’t forget to think about cause of atrial fib/flutter and treat!Don’t forget to think about cause of atrial fib/flutter and treat!


““Convert or Not to Convert”….Convert or Not to Convert”…. > 48 hrs increased risk of embolic (however > 48 hrs increased risk of embolic (however

Rosen’s mentions can convert up to 72 hrs)Rosen’s mentions can convert up to 72 hrs) Chemical vs ElectricalChemical vs Electrical

Electrical Electrical 50 – 100 J to start50 – 100 J to start No associated risk of malignant ventricular No associated risk of malignant ventricular

dysrhythmias on pts with dig unless evidence of dysrhythmias on pts with dig unless evidence of toxicitytoxicity

Can premedicate with rate slowing agent (Ca++)Can premedicate with rate slowing agent (Ca++) ChemicalChemical

Amiodarone 5mg/kg IV, over 15 – 20 minutesAmiodarone 5mg/kg IV, over 15 – 20 minutes Other options…procainamide, ibutilideOther options…procainamide, ibutilide

Don’t forget about Anticoagulation!Don’t forget about Anticoagulation!


Atrial FlutterAtrial Flutter ““sawtooth” pattern best seen in II, III, aVF, sawtooth” pattern best seen in II, III, aVF,

V1, V2V1, V2 Usually 2:1 or 4:1 but any ratio can be seenUsually 2:1 or 4:1 but any ratio can be seen Atrial rates ~300/min (classical)Atrial rates ~300/min (classical) Ventricular rates ~ 150 bpm (classical)Ventricular rates ~ 150 bpm (classical) Narrow ComplexNarrow Complex Causes: CHF, Underlying heart disease, Causes: CHF, Underlying heart disease,

Valve dysfxn, MetabolicValve dysfxn, Metabolic

TachydysrhythmiasTachydysrhythmias Tx: stable vs unstableTx: stable vs unstable

Ca++ (Diltiazem may better b/c of less hypotension Ca++ (Diltiazem may better b/c of less hypotension and inotropic effect)/B-blockerand inotropic effect)/B-blocker

Digitalis (0.5mg IV initial and repeat doses q1-2hrs in Digitalis (0.5mg IV initial and repeat doses q1-2hrs in 0.25mg increments until effect or total dose = 1.5mg)0.25mg increments until effect or total dose = 1.5mg)

Magnesium (2 – 4 g IV)Magnesium (2 – 4 g IV) Cardioversion (unstable or recurrent)Cardioversion (unstable or recurrent)

Low energy cardioversion 25 – 50 JLow energy cardioversion 25 – 50 J Determine cause!! Determine cause!!

PitfallsPitfalls Watch out for possibility of accessory pathway (eg. Watch out for possibility of accessory pathway (eg.

Ventricular rates of > 200 bpm since normal AV nodal Ventricular rates of > 200 bpm since normal AV nodal pathways are unlikely to allow rates that high)pathways are unlikely to allow rates that high)

Avoid primary AV nodal blocking agents in these Avoid primary AV nodal blocking agents in these instances since may precipitate Vfib instances since may precipitate Vfib

Should investigate with EP studies Should investigate with EP studies



Case # 2Case # 2 40 yr old male “feeling funny in chest”. 40 yr old male “feeling funny in chest”. PMHx: HealthyPMHx: Healthy Meds: noneMeds: none Vitals: HR 200, BP 130/80, Sats 98% Vitals: HR 200, BP 130/80, Sats 98%

RA, RA,



Narrow Complex Tachycardias (that Narrow Complex Tachycardias (that are not Afib/Aflutter)are not Afib/Aflutter) QRS < 0.12 sec and ventricular rate of QRS < 0.12 sec and ventricular rate of

> 100> 100 P waves usually “hidden” due to fast P waves usually “hidden” due to fast

raterate Regular Regular Stable vs UnstableStable vs Unstable


Sinus TachycardiaSinus Tachycardia Don’t forget to think about the cause!!!Don’t forget to think about the cause!!! Response to physiological stress due to Response to physiological stress due to

body trying to increase cardiac outputbody trying to increase cardiac output Eg. Sepsis, PE, shock…Eg. Sepsis, PE, shock…

Tx: treat the cause!!Tx: treat the cause!!


Atrial TachycardiaAtrial Tachycardia Tachycardia originating above nonsinus Tachycardia originating above nonsinus

focus above the AV nodefocus above the AV node Gradual or abruptGradual or abrupt Hallmark: narrow complex tachycardia Hallmark: narrow complex tachycardia

with each QRS preceded by a P wave with each QRS preceded by a P wave that is morphologically different from that is morphologically different from the sinus P wavethe sinus P wave


Case #3Case #3 75 yr old male sent in by GP because of 75 yr old male sent in by GP because of

lightheadedness and dizziness following lightheadedness and dizziness following progressive SOB and productive cough for 2 progressive SOB and productive cough for 2 days.days.

PMHx: COPDPMHx: COPD Meds: “Damm oxygen at home…makes me Meds: “Damm oxygen at home…makes me

feel like a dog on a leash…AND I can’t feel like a dog on a leash…AND I can’t smoke with it on!!”smoke with it on!!”

Vitals: 120 HR irregular, 160/90, O2 88% on Vitals: 120 HR irregular, 160/90, O2 88% on 1 L1 L


ECGECG

TachydysrhythmiasTachydysrhythmias Multifocal Atrial TachycardiaMultifocal Atrial Tachycardia

““wandering atrial pacemaker”wandering atrial pacemaker” ECG findingsECG findings

At least 3 morphologically distinct P wavesAt least 3 morphologically distinct P waves Changing P-P, P-R, and R-R intervalsChanging P-P, P-R, and R-R intervals Atrial rhythm usually b/w 100 – 180 bpmAtrial rhythm usually b/w 100 – 180 bpm

Most commonly in elderly patientsMost commonly in elderly patients Causes: chronic lung problems, pulmonary Causes: chronic lung problems, pulmonary

diseasedisease TX: treat underlying problem (usually resp)TX: treat underlying problem (usually resp)

Mg 2 g IV over 60 secs then 1 – 2 g/h infusionMg 2 g IV over 60 secs then 1 – 2 g/h infusion Verapamil 5 – 10 mg IVVerapamil 5 – 10 mg IV B-blockers (watch out for theroretical risk of B-blockers (watch out for theroretical risk of

increasing pulmonary issues)increasing pulmonary issues)


Supraventricular TachycardiaSupraventricular Tachycardia SVT: any tachycardia originating above the SVT: any tachycardia originating above the

ventricles; includes sinus tach, Afib, aflut, PSVT, ventricles; includes sinus tach, Afib, aflut, PSVT, junctional tachjunctional tach

PSVT: a type of SVT; two causes…….PSVT: a type of SVT; two causes……. AVNRT: AV node Re-entrant Tachycardia (also called AVNRT: AV node Re-entrant Tachycardia (also called

Paroxysmal Junctional Tach) - AV node reentryParoxysmal Junctional Tach) - AV node reentry HR usually less than 200HR usually less than 200 P wave usually buriedP wave usually buried

AVRT: AV Re-entrant Tachycardia - re-entry b/w atria AVRT: AV Re-entrant Tachycardia - re-entry b/w atria and ventricle due to accessory pathwayand ventricle due to accessory pathway

Suspect if HR > 200Suspect if HR > 200 WPW most commonWPW most common


Tx:Tx: Stable vs UnstableStable vs Unstable Vagal maneuversVagal maneuvers AdenosineAdenosine CardioversionCardioversion Other options: Amio, CCB, Other options: Amio, CCB,

procainamide…procainamide…


Case # 3Case # 3 17 yr old male with episodic “racing 17 yr old male with episodic “racing

heart” for years. No parents with him. heart” for years. No parents with him. States he has had this before and sees a States he has had this before and sees a cardiologist but can’t remember who.cardiologist but can’t remember who.

Vitals: HR 60, BP 110/60, Sats 98% RAVitals: HR 60, BP 110/60, Sats 98% RA



WPWWPW Most common accessory pathway syndromeMost common accessory pathway syndrome Hallmark: PSVT at 150 – 300 bpmHallmark: PSVT at 150 – 300 bpm Loss of normal AV conduction restraintLoss of normal AV conduction restraint 70 % of pts have no underlying heart disease70 % of pts have no underlying heart disease Classic 3 featuresClassic 3 features

Short PR interval ( < 0.12 sec)Short PR interval ( < 0.12 sec) QRS > 0.10QRS > 0.10 ““Delta” wave (early activation of myocardium)Delta” wave (early activation of myocardium)


OrthodromicOrthodromic Narrow QRSNarrow QRS Delta wave absentDelta wave absent Down through AV Down through AV

nodenode Up through Up through

accessory pathwayaccessory pathway

AntidromicAntidromic Wide QRSWide QRS Delta wave presentDelta wave present Down through Down through

accessory pathwayaccessory pathway Up through AV Up through AV

nodenode

TachydysrhythmiasTachydysrhythmias WPWWPW

TreatmentTreatment Stable vs UnstableStable vs Unstable Depends on 3 observations:Depends on 3 observations:

Symptoms of instabilitySymptoms of instability QRS duration or Delta wave presenceQRS duration or Delta wave presence QRS regularity or irregularityQRS regularity or irregularity

Regular OrthodromicRegular Orthodromic Most commonMost common Treat same as SVTTreat same as SVT

Regular Antidromic or any irregular rhythmRegular Antidromic or any irregular rhythm High risk of Vfib (esp when RR interval < 0.20)High risk of Vfib (esp when RR interval < 0.20) Avoid AV nodal blocking drugs (CCB, BB, dig, adenosine)Avoid AV nodal blocking drugs (CCB, BB, dig, adenosine) Procainamide is drug of choice or cardioversion if > 250 Procainamide is drug of choice or cardioversion if > 250

bpmbpm Amiodarone can also be consideredAmiodarone can also be considered


Wide Complex TachycardiasWide Complex Tachycardias > 100 bpm and QRS > 0.12 sec> 100 bpm and QRS > 0.12 sec 2 groups2 groups

VentricularVentricular SVT with aberrancySVT with aberrancy

Must determine difference in order to Must determine difference in order to treat properlytreat properly

Use focused hx, physical exam, and Use focused hx, physical exam, and ECG tracingECG tracing

Distinguishing VT from SVT Distinguishing VT from SVT with aberrancy with aberrancy

SVT can occasionally present as an SVT can occasionally present as an unknown wide-complex tachycardia unknown wide-complex tachycardia if if occurs in the presence of:if if occurs in the presence of: Preexisting bundle branch blockPreexisting bundle branch block Rate related bundle branch blockRate related bundle branch block An accessory pathwayAn accessory pathway Treatment with class IA or IC Treatment with class IA or IC

antiarrhythmicsantiarrhythmics

Distinguishing VT from SVT Distinguishing VT from SVT with aberrancywith aberrancy

VT accounts for ~80% of all cases of regular VT accounts for ~80% of all cases of regular wide-complex tachycardias, and ~95% of all wide-complex tachycardias, and ~95% of all cases of regular wide-complex tachycardias cases of regular wide-complex tachycardias which occur in patients with a history of MI.which occur in patients with a history of MI.

One of the most common lethal errors made One of the most common lethal errors made in arrhythmia diagnosis is to mistake VT for in arrhythmia diagnosis is to mistake VT for SVT and treat with verapamil, diltiazem, and SVT and treat with verapamil, diltiazem, and adenosine, all of which can precipitate adenosine, all of which can precipitate ventricular fibrillation in patients in VT, ventricular fibrillation in patients in VT, even if initially stable.even if initially stable.

TachydysrhythmiasTachydysrhythmias Ventricular TachycardiaVentricular Tachycardia

> 50 yrs> 50 yrs Hx of MI, CHF, CABG, Hx of MI, CHF, CABG,

ASHDASHD Mitral Valve ProlapseMitral Valve Prolapse Prev hx of VTPrev hx of VT Cannon “A” wavesCannon “A” waves Variation in arterial pulseVariation in arterial pulse Variable first heart soundVariable first heart sound Fusion beatsFusion beats AV dissociationAV dissociation QRS > 0.14 secQRS > 0.14 sec Extreme LAD Extreme LAD No response to vagal No response to vagal

maneuversmaneuvers V1: R, qR or RSV1: R, qR or RS V6: S, rS, or qRV6: S, rS, or qR

SVT with AberrancySVT with Aberrancy < 36 yrs< 36 yrs No hx of heart diseaseNo hx of heart disease Mitral valve prolapseMitral valve prolapse Prev hx of SVTPrev hx of SVT No cannon “A” wavesNo cannon “A” waves Absence of variabilityAbsence of variability No variable first heart No variable first heart

soundsound No fusion beatsNo fusion beats No AV dissociationNo AV dissociation QRS < 0.14 (usually)QRS < 0.14 (usually) Normal Axis Normal Axis Vagal maneuversVagal maneuvers V1: rsR’V1: rsR’ V6: qRsV6: qRs

A-V Dissociation, Fusion, A-V Dissociation, Fusion, and and

Capture Beats in VTCapture Beats in VT

Fisch C. Electrocardiography of Arrhythmias. 1990;134.

ECTOPY FUSION CAPTURE

V1 E F C


Brugada CriteriaBrugada Criteria


Morphology Criteria in leads V1 and Morphology Criteria in leads V1 and V6V6

The Brugada CriteriaThe Brugada Criteria

Table I.

Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm

Step 1. Is there absence of an RS complex in all precordial leads V1 – V6?

If yes, then the rhythm is VT. Sens 0.21 Spec 1.0

Step 2. Is the interval from the onset of the R wave to the nadir of the Swave greater than 100 msec in any precordial leads?


Step 3. Is there AV dissociation?

If yes, then the rhythm is VT.

Sens 0.82 Spec 0.98

Step 4. Are morphology criteria for VT present? See Table II.


Morphology Criteria for Morphology Criteria for VTVT

Table II.

Morphology Criteria for VT

Right bundle type requires waveform from both V1 and V6.

V1 V6

Monophasic R wave QS or QR

QR or RS R/S <1

Left bundle type requires any of the below morphologies.

V1or V2 V6

R wave > 30 msec

Notched downstroke S wave.

Greater than 60msec nadir S wave.

QR or QS

Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex.Circulation 1991; 83:1649-59.

TachydysrhythmiasTachydysrhythmias Brugada P, et al: A new approach to the Brugada P, et al: A new approach to the

differential diagnosis of regular tachycardia differential diagnosis of regular tachycardia with wide QRS complex. Circulation with wide QRS complex. Circulation 83:1649. 199183:1649. 1991

Any “yes” is VTAny “yes” is VT Can only be used with regular tachycardiasCan only be used with regular tachycardias Later studies showed poor sensitivity and Later studies showed poor sensitivity and

specificity (Isenhour et al, Academic Emerg specificity (Isenhour et al, Academic Emerg Med 2000: 7 (7): 769 – 773)Med 2000: 7 (7): 769 – 773)

Best to think if new onest wide complex Best to think if new onest wide complex tachycardia is VT until proven otherwise.tachycardia is VT until proven otherwise.


Case # 4Case # 4 60 yr old male farmer with SOB and 60 yr old male farmer with SOB and

chest pain brought by wifechest pain brought by wife PMx: “sugar diabetes” and “problems PMx: “sugar diabetes” and “problems

with the ticker”with the ticker” Meds: “All I know is what the druggist Meds: “All I know is what the druggist

gives me once a month is what I take…”gives me once a month is what I take…” Has a pulseHas a pulse



Ventricular TachycardiasVentricular Tachycardias VTachVTach

MonomorphicMonomorphic PolymorphicPolymorphic

Vfib/flutterVfib/flutter


Monomorphic VTachMonomorphic VTach Consistent QRS complexesConsistent QRS complexes Seen in CAD/IHD, lytes abnormalities, Seen in CAD/IHD, lytes abnormalities,

hypoxemiahypoxemia Tx: stableTx: stable

LidocaineLidocaine CardioversionCardioversion Procainamide, Amio, MagnesiumProcainamide, Amio, Magnesium


Case # 5Case # 5 80 yr old female feeling weak and dizzy, 80 yr old female feeling weak and dizzy,

EMS patch in rhythm strip because EMS patch in rhythm strip because unsure……unsure……


TachydysrhythmiasTachydysrhythmias Polymorphic VtachPolymorphic Vtach

QRS of varying morphologyQRS of varying morphology More severe diseaseMore severe disease Torsades de PointesTorsades de Pointes

Clinical CriteriaClinical Criteria Ventricular rate > 200 bpmVentricular rate > 200 bpm QRS axis undulatingQRS axis undulating ParoxysmalParoxysmal

Often in setting of prolonged QT intervalOften in setting of prolonged QT interval Hypokalemia, hypomagnesemiaHypokalemia, hypomagnesemia Tx: based on correcting underlying abnormalities Tx: based on correcting underlying abnormalities

and increasing HRand increasing HR MagnesiumMagnesium Overdrive pacingOverdrive pacing IsoproterenolIsoproterenol


Wide Complex Tachycardia of Wide Complex Tachycardia of Unknown OriginUnknown Origin Assume VT until proven otherwiseAssume VT until proven otherwise Management same as for monomorphic Management same as for monomorphic

VTVT


Take home points:Take home points: Stable vs UnstableStable vs Unstable

Remember this is patient specific.Remember this is patient specific. Eg. Elderly pt in afib with bp of 110/60 could Eg. Elderly pt in afib with bp of 110/60 could

be unstable if they are regularly 160/90.be unstable if they are regularly 160/90.

Review common ED presentations of Review common ED presentations of tachydysrhythmiastachydysrhythmias

Understand the basic concepts behind Understand the basic concepts behind the drugs we choosethe drugs we choose

Review, Review, Review……Review, Review, Review……

Tachydysrhymias Stefan Da Silva Oct 19 th 2006 Special Guest: Dr. Phil Ukrainetz With a little help from Drs. R. Hall and D. Peterson.

Documents

membrane potential

mv potential

resting potential

refractory phase

action potential durationeg

result of spontaneous

mv membrane

initial route