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Tachydysrhymias
Stefan Da Silva
Oct 19th 2006
Special Guest: Dr. Phil Ukrainetz
With a little help from Drs. R. Hall and D. Peterson
Tachydysrhythmias
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
Dysrhythmia: any abnormality in cardiac
rhythm
Anatomy
SA node
 AV node
 Bundle Branches
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Tachydysrhythmias
Tachydysrhythmias

Cardiac Electrophysiology (the very basics!)

Na/K pump
3 Na OUT
 2 K IN


This generates approx 10 mV potential across membrane
The flow of K down the concentration gradient toward
the ECF generates another 80 mV
 Ca is also exchanged for Na along membrane via osmotic
gradient

= 90 mV membrane resting potential
Tachydysrhythmias
Tachydysrhythmias
Tachydysrhythmias
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Mechanisms for Dysrhythmias
Altered Automaticity
 Re-entry
 Triggered Mechanisms
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Tachydysrhythmias
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Altered Automaticity
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Impulse related
Can occur in multiple settings (ischemia, electrolyte
abnormalities, drugs…)
Can be a result of spontaneous phase 4 depolarization in
“non-pacemaker” cells (abnormal automaticity)


Eg. VT after MI
Increase in the slope of depolarization causing it to be more
positive/closer to threshold (enhanced automaticity)

Eg. Idioventricular rhythm after MI

Enhanced automaticity as a result of catecholamine increase stimulating
non-SA nodal pacemakers.
Tachydysrhythmias
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Re-entry
Conduction related
 Most common cause of narrow complex rhythms
(50% - 80%)
 Need 3 conditions for re-entry

1) Pathway  2 paths available
 2) Unequal responsiveness between routes
 3) Decrease in conduction of one route
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Tachydysrhythmias
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What happens???

Dysfunction at the junction
Impulse finds one route “dysfunctional” (ie. in refractory
phase) therefore travels down alternate route and circles
back up towards initial route (retrograde) since it has
recovered from refractory period.
 Can result in narrow complex tachycardia

Tachydysrhythmias
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Triggered
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Result of “afterdepolarization”  fluctuations in membrane
potential that occur as the resting potential is approached
which may precipitate another depolarization
Dependant on heart rate for propagation
Can be either early or late afterdepolarizations.
Late: enhanced by faster heart rates. eg. Intracellular Ca
overload in reperfusion therapy post MI can cause
dysrhythmias such as VT, bigeminy, junctional rhythms
Early: enhanced by slower heart rates. eg. Torsades de
pointes
Triggered Activity
(early afterdepolarizations)
Early afterdepolarizations occur during
either phase 2 or
phase 3 of the action
potential, and are
seen most commonly
in QT prolongation.
Triggered Activity
(late afterdepolarizations)
Late afterdepolarizations occur shortly
after completion of
repolarization, and
are seen most
commonly in digitalis
intoxication and high
catecholamine states.
Tachydysrhythmias


Antidysrhythmic Drugs
Class I
Na (fast) channel blockers
 “Membrane stabilizing”
 Anti-ectopic effects
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IA: slows deplolarization and conduction. Prolong
repolarization and AP duration
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Eg. Procainamide: dosage  20 – 30 mg/min until
termination of dysrhythmia, decrease in BP, widening QRS
greater than 50% of initial width or total dose of 18 – 20
mg/kg adminstered (can be given up to 50 mg/min in
“urgent” situations..)
Maintenance: 1 – 4 mg/min
Can be given orally as outpt.
Tachydysrhythmias

IB: slows depolarization and conduction. Shorten
repolarization and action potential duration


Eg. Lidocaine: Dosing
 1.0 - 1.5mg/kg IV single dose (if refractory can repeat dose
0.5 – 0.75 mg/kg IV q 5 – 10mins…max dose 3 mg/kg)
IC: markedly slows depolarization and conduction.
Prolongs repolarization and action potential duration

Eg. Propafenone
 1 – 2 mg/kg at 10mg/min….infuse slowly
Tachydysrhythmias

Class II
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B-Blockers (all the “ol’s”…propanolol, esmolol, metoprolol)
Slow SA node rate and AV conduction
Prolong action potential
Depress conduction in ischemic myocardial tissues
Class III
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Prolong action potential and refractory period
Exhibit antifibrillartory effects
Eg. Amiodarone

Dosing:
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Arrest: 300mg IV push then 150 mg IV in 3 to 5 mins..max dose in 24
hrs is 2.2g
Arrhythmias: 150 mg IV over 1st 10 minutes can repeat q 10 min as
needed to max dose.
Tachydysrhythmias

Class IV
Slow Ca channel blockers
 Depress anterograde conduction through AV node.
 Eg. Diltiazem


Dosing: 15 – 20 mg IV over 2 minutes, can repeat at 20 – 25 mg
IV after 15 minutes
 Can give Calcium prior to decrease hypotensive effects
Tachydysrhythmias

Approach
ABC’s
 Stable vs non-stable
 ECG

Wide vs Narrow!!!
 Regular vs Irregular
 P waves vs No P waves


Old Chart (old ECG’s extremely helpful)
Tachydysrhythmias

What do you want to know?


Stable or not stable
Stable…now what?

Have time to do focussed hx and physical

Hx:
timing, palpitations, dizziness, chest pain, SOB, syncope etc
 Previous hx of similar
 Medications
Physical
 Evidence of end-organ perfusion/alteration in cognition
 Regular cardio-pulmonary exam.
ECG
Interventions
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Tachydysrhythmias
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Case #1
76 yr old male presenting with 1 day hx of heart
“racing” and mild breathless
 PMHx: “some heart problems”
 Meds: “…half a blue pill for BP and water pill or
something like that…”
 Vitals: fluctuating HR 120 – 150, BP 160/96, Sat
96% RA, 36.5 temp
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Tachydysrhythmias
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CASE #1
Tachydysrhythmias
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Atrial Fibrillation
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“chaos”
Irregularly irregular
No distinct “P” waves
Narrow Complex
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Ashman Phenomenon: isolated/repeated aberrant ventricular conduction in
RBBB pattern
Atrial rates of ~300 bpm
Ventricular rates ~ 150 – 200
Can be dangerous in patients with LV dysfunction as high likelihood of
going into heart failure if in Afib

If > 200 bpm beware of accessory pathway and predisposition to Vfib
Tachydysrhythmias
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Causes: IHD, pericarditis, thyroid dysfunction, cardiomyopathy, PE, CHF
Tx:
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Stable vs unstable
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Rate control
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Immediate cardioversion if unstable
Preserved vs unpreserved ventricular function
Ca++/B-blockers
If in doubt Diltiazem can be used for both normal and impaired LV function (ACLS)
Rhythm control
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Duration
Chemical vs Electrical
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Anticoagulation
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Amiodarone
Anticoag clinics
Afib clinic here in Calgary
Don’t forget to think about cause of atrial fib/flutter and treat!
Tachydysrhythmias

“Convert or Not to Convert”….
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> 48 hrs increased risk of embolic (however Rosen’s
mentions can convert up to 72 hrs)
Chemical vs Electrical
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Electrical
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Chemical
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50 – 100 J to start
No associated risk of malignant ventricular dysrhythmias on pts with dig
unless evidence of toxicity
Can premedicate with rate slowing agent (Ca++)
Amiodarone 5mg/kg IV, over 15 – 20 minutes
Other options…procainamide, ibutilide
Don’t forget about Anticoagulation!
Tachydysrhythmias
Atrial Flutter
“sawtooth” pattern best seen in II, III, aVF, V1, V2
 Usually 2:1 or 4:1 but any ratio can be seen
 Atrial rates ~300/min (classical)
 Ventricular rates ~ 150 bpm (classical)
 Narrow Complex
 Causes: CHF, Underlying heart disease, Valve dysfxn,
Metabolic
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Tachydysrhythmias
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Tx: stable vs unstable
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Ca++ (Diltiazem may better b/c of less hypotension and inotropic
effect)/B-blocker
Digitalis (0.5mg IV initial and repeat doses q1-2hrs in 0.25mg increments
until effect or total dose = 1.5mg)
Magnesium (2 – 4 g IV)
Cardioversion (unstable or recurrent)
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Low energy cardioversion 25 – 50 J
Determine cause!!
Pitfalls

Watch out for possibility of accessory pathway (eg. Ventricular rates of > 200
bpm since normal AV nodal pathways are unlikely to allow rates that high)
 Avoid primary AV nodal blocking agents in these instances since may
precipitate Vfib
 Should investigate with EP studies
Tachydysrhythmias
Tachydysrhythmias

Case # 2
40 yr old male “feeling funny in chest”.
 PMHx: Healthy
 Meds: none
 Vitals: HR 200, BP 130/80, Sats 98% RA,
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Tachydysrhythmias
Tachydysrhythmias

Narrow Complex Tachycardias (that are not
Afib/Aflutter)
QRS < 0.12 sec and ventricular rate of > 100
 P waves usually “hidden” due to fast rate
 Regular
 Stable vs Unstable
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Tachydysrhythmias
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Sinus Tachycardia
Don’t forget to think about the cause!!!
 Response to physiological stress due to body trying
to increase cardiac output
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Eg. Sepsis, PE, shock…
Tx: treat the cause!!
Tachydysrhythmias
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Atrial Tachycardia
Tachycardia originating above nonsinus focus above
the AV node
 Gradual or abrupt
 Hallmark: narrow complex tachycardia with each
QRS preceded by a P wave that is morphologically
different from the sinus P wave
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Tachydysrhythmias

Case #3
75 yr old male sent in by GP because of
lightheadedness and dizziness following progressive
SOB and productive cough for 2 days.
 PMHx: COPD
 Meds: “Damm oxygen at home…makes me feel like
a dog on a leash…AND I can’t smoke with it on!!”
 Vitals: 120 HR irregular, 160/90, O2 88% on 1 L

Tachydysrhythmias
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ECG
Tachydysrhythmias
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Multifocal Atrial Tachycardia
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“wandering atrial pacemaker”
ECG findings
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At least 3 morphologically distinct P waves
Changing P-P, P-R, and R-R intervals
Atrial rhythm usually b/w 100 – 180 bpm
Most commonly in elderly patients
Causes: chronic lung problems, pulmonary disease
TX: treat underlying problem (usually resp)



Mg 2 g IV over 60 secs then 1 – 2 g/h infusion
Verapamil 5 – 10 mg IV
B-blockers (watch out for theroretical risk of increasing pulmonary
issues)
Tachydysrhythmias
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Supraventricular Tachycardia
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SVT: any tachycardia originating above the ventricles;
includes sinus tach, Afib, aflut, PSVT, junctional tach
PSVT: a type of SVT; two causes…….
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AVNRT: AV node Re-entrant Tachycardia (also called Paroxysmal
Junctional Tach) - AV node reentry
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HR usually less than 200
P wave usually buried
AVRT: AV Re-entrant Tachycardia - re-entry b/w atria and ventricle
due to accessory pathway
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Suspect if HR > 200
WPW most common
Tachydysrhythmias

Tx:
Stable vs Unstable
 Vagal maneuvers
 Adenosine
 Cardioversion
 Other options: Amio, CCB, procainamide…

Tachydysrhythmias

Case # 3
17 yr old male with episodic “racing heart” for years.
No parents with him. States he has had this before
and sees a cardiologist but can’t remember who.
 Vitals: HR 60, BP 110/60, Sats 98% RA

Tachydysrhythmias
Tachydysrhythmias

WPW
Most common accessory pathway syndrome
 Hallmark: PSVT at 150 – 300 bpm
 Loss of normal AV conduction restraint
 70 % of pts have no underlying heart disease
 Classic 3 features

Short PR interval ( < 0.12 sec)
 QRS > 0.10
 “Delta” wave (early activation of myocardium)
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Tachydysrhythmias
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Orthodromic
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Narrow QRS
Delta wave absent
Down through AV node
Up through accessory
pathway
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Antidromic
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Wide QRS
Delta wave present
Down through accessory
pathway
Up through AV node
Tachydysrhythmias
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WPW
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Treatment
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Stable vs Unstable
Depends on 3 observations:
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Regular Orthodromic
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Symptoms of instability
QRS duration or Delta wave presence
QRS regularity or irregularity
Most common
Treat same as SVT
Regular Antidromic or any irregular rhythm
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High risk of Vfib (esp when RR interval < 0.20)
Avoid AV nodal blocking drugs (CCB, BB, dig, adenosine)
Procainamide is drug of choice or cardioversion if > 250 bpm
Amiodarone can also be considered
Tachydysrhythmias

Wide Complex Tachycardias
> 100 bpm and QRS > 0.12 sec
 2 groups

Ventricular
 SVT with aberrancy

Must determine difference in order to treat properly
 Use focused hx, physical exam, and ECG tracing

Distinguishing VT from SVT with
aberrancy

SVT can occasionally present as an unknown
wide-complex tachycardia if if occurs in the
presence of:
Preexisting bundle branch block
 Rate related bundle branch block
 An accessory pathway
 Treatment with class IA or IC antiarrhythmics

Distinguishing VT from SVT with
aberrancy

VT accounts for ~80% of all cases of regular widecomplex tachycardias, and ~95% of all cases of regular
wide-complex tachycardias which occur in patients with
a history of MI.

One of the most common lethal errors made in
arrhythmia diagnosis is to mistake VT for SVT and
treat with verapamil, diltiazem, and adenosine, all of
which can precipitate ventricular fibrillation in patients
in VT, even if initially stable.
Tachydysrhythmias
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Ventricular Tachycardia
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> 50 yrs
Hx of MI, CHF, CABG, ASHD
Mitral Valve Prolapse
Prev hx of VT
Cannon “A” waves
Variation in arterial pulse
Variable first heart sound
Fusion beats
AV dissociation
QRS > 0.14 sec
Extreme LAD
No response to vagal maneuvers
V1: R, qR or RS
V6: S, rS, or qR
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SVT with Aberrancy
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< 36 yrs
No hx of heart disease
Mitral valve prolapse
Prev hx of SVT
No cannon “A” waves
Absence of variability
No variable first heart sound
No fusion beats
No AV dissociation
QRS < 0.14 (usually)
Normal Axis
Vagal maneuvers
V1: rsR’
V6: qRs
A-V Dissociation, Fusion, and
Capture Beats in VT
V1
E
ECTOPY
F
C
FUSION
Fisch C. Electrocardiography of Arrhythmias. 1990;134.
CAPTURE
Tachydysrhythmias

Brugada Criteria
Tachydysrhythmias

Morphology Criteria in leads V1 and V6
The 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 S
wave greater than 100 msec in any precordial leads?
If yes, then the rhythm is VT.

Sens 0.66 Spec 0.98
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.
If yes, then the rhythm is VT.

Sens 0.99 Spec 0.97
Morphology Criteria for VT
Table II.
Morphology Criteria for VT
Right bundle type requires waveform from both V1 and V6.
V1
V6
Monophasic R wave
QR
or
QS
RS
or
QR
R/S <1
Left bundle type requires any of the below morphologies.
V1or V2
V6
R wave > 30 msec
QR
or
QS
Notched downstroke
S wave.
Greater than 60msec
nadir S wave.
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.
Tachydysrhythmias
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Brugada P, et al: A new approach to the differential
diagnosis of regular tachycardia with wide QRS
complex. Circulation 83:1649. 1991
Any “yes” is VT
Can only be used with regular tachycardias
Later studies showed poor sensitivity and specificity
(Isenhour et al, Academic Emerg Med 2000: 7 (7): 769
– 773)
Best to think if new onest wide complex tachycardia is
VT until proven otherwise.
Tachydysrhythmias

Case # 4
60 yr old male farmer with SOB and chest pain
brought by wife
 PMx: “sugar diabetes” and “problems with the
ticker”
 Meds: “All I know is what the druggist gives me
once a month is what I take…”
 Has a pulse

Tachydysrhythmias
Tachydysrhythmias

Ventricular Tachycardias

VTach

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Monomorphic
Polymorphic
Vfib/flutter
Tachydysrhythmias

Monomorphic VTach
Consistent QRS complexes
 Seen in CAD/IHD, lytes abnormalities, hypoxemia
 Tx: stable

Lidocaine
 Cardioversion
 Procainamide, Amio, Magnesium

Tachydysrhythmias

Case # 5

80 yr old female feeling weak and dizzy, EMS patch
in rhythm strip because unsure……
Tachydysrhythmias
Tachydysrhythmias

Polymorphic Vtach
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QRS of varying morphology
More severe disease
Torsades de Pointes
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Clinical Criteria
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Ventricular rate > 200 bpm
QRS axis undulating
Paroxysmal
Often in setting of prolonged QT interval
Hypokalemia, hypomagnesemia
Tx: based on correcting underlying abnormalities and increasing HR



Magnesium
Overdrive pacing
Isoproterenol
Tachydysrhythmias

Wide Complex Tachycardia of Unknown Origin
Assume VT until proven otherwise
 Management same as for monomorphic VT

Tachydysrhythmias

Take home points:

Stable vs Unstable

Remember this is patient specific.

Eg. Elderly pt in afib with bp of 110/60 could be unstable
if they are regularly 160/90.
Review common ED presentations of
tachydysrhythmias
 Understand the basic concepts behind the drugs we
choose
 Review, Review, Review……
