Tachydysrhymias

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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

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Tachydysrhythmias

• Dysrhythmia any abnormality in cardiac rhythm
• Anatomy
• SA node
• AV node
• Bundle Branches

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Tachydysrhythmias
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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

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Tachydysrhythmias
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Tachydysrhythmias
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Tachydysrhythmias

• Mechanisms for Dysrhythmias
• Altered Automaticity
• Re-entry
• Triggered Mechanisms

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Tachydysrhythmias

• Altered Automaticity
• 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.

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Tachydysrhythmias

• 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

• 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

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Tachydysrhythmias

• Triggered
• 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

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Triggered Activity(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.
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Triggered Activity(late afterdepolarizations)
Late afterdepolar-izations occur shortly after
completion of repolarization, and are seen most
commonly in digitalis intoxication and high
catecholamine states.
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Tachydysrhythmias

• Antidysrhythmic Drugs
• Class I
• Na (fast) channel blockers
• Membrane stabilizing
• Anti-ectopic effects
• IA slows deplolarization and conduction.
  Prolong repolarization and AP duration
• 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.

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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 10minsmax
  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

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Tachydysrhythmias

• Class II
• B-Blockers (all the olspropanolol, esmolol,
  metoprolol)
• Slow SA node rate and AV conduction
• Prolong action potential
• Depress conduction in ischemic myocardial tissues
• Class III
• Prolong action potential and refractory period
• Exhibit antifibrillartory effects
• Eg. Amiodarone
• Dosing
• 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.

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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

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Tachydysrhythmias

• Approach
• ABCs
• Stable vs non-stable
• ECG
• Wide vs Narrow!!!
• Regular vs Irregular
• P waves vs No P waves
• Old Chart (old ECGs extremely helpful)

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Tachydysrhythmias

• What do you want to know?
• Stable or not stable
• Stablenow 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

• 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

• CASE 1

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Tachydysrhythmias

• Atrial Fibrillation
• chaos
• Irregularly irregular
• No distinct P waves
• Narrow Complex
• 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 gt 200 bpm beware of accessory pathway and
  predisposition to Vfib

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Tachydysrhythmias

• Causes IHD, pericarditis, thyroid dysfunction,
  cardiomyopathy, PE, CHF
• Tx
• Stable vs unstable
• Immediate cardioversion if unstable
• Rate control
• 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
• Duration
• Chemical vs Electrical
• Amiodarone
• Anticoagulation
• Anticoag clinics
• Afib clinic here in Calgary
• Dont forget to think about cause of atrial
  fib/flutter and treat!

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Tachydysrhythmias

• Convert or Not to Convert.
• gt 48 hrs increased risk of embolic (however
  Rosens mentions can convert up to 72 hrs)
• Chemical vs Electrical
• Electrical
• 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)
• Chemical
• Amiodarone 5mg/kg IV, over 15 20 minutes
• Other optionsprocainamide, ibutilide
• Dont forget about Anticoagulation!

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Tachydysrhythmias

• Atrial Flutter
• sawtooth pattern best seen in II, III, aVF, V1,
  V2
• Usually 21 or 41 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

• Tx stable vs unstable
• 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)
• Low energy cardioversion 25 50 J
• Determine cause!!
• Pitfalls
• Watch out for possibility of accessory pathway
  (eg. Ventricular rates of gt 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

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Tachydysrhythmias
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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
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Tachydysrhythmias

• Narrow Complex Tachycardias (that are not
  Afib/Aflutter)
• QRS lt 0.12 sec and ventricular rate of gt 100
• P waves usually hidden due to fast rate
• Regular
• Stable vs Unstable

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Tachydysrhythmias

• Sinus Tachycardia
• Dont forget to think about the cause!!!
• Response to physiological stress due to body
  trying to increase cardiac output
• Eg. Sepsis, PE, shock
• Tx treat the cause!!

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Tachydysrhythmias

• 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 homemakes me feel like a
  dog on a leashAND I cant smoke with it on!!
• Vitals 120 HR irregular, 160/90, O2 88 on 1 L

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Tachydysrhythmias

• ECG

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Tachydysrhythmias

• Multifocal Atrial Tachycardia
• wandering atrial pacemaker
• ECG findings
• 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)

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Tachydysrhythmias

• Supraventricular Tachycardia
• SVT any tachycardia originating above the
  ventricles includes sinus tach, Afib, aflut,
  PSVT, junctional tach
• PSVT a type of SVT two causes.
• AVNRT AV node Re-entrant Tachycardia (also
  called Paroxysmal Junctional Tach) - AV node
  reentry
• 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
• Suspect if HR gt 200
• WPW most common

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Tachydysrhythmias

• Tx
• Stable vs Unstable
• Vagal maneuvers
• Adenosine
• Cardioversion
• Other options Amio, CCB, procainamide

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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 cant
  remember who.
• Vitals HR 60, BP 110/60, Sats 98 RA

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Tachydysrhythmias
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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 ( lt 0.12 sec)
• QRS gt 0.10
• Delta wave (early activation of myocardium)

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Tachydysrhythmias

• Orthodromic
• Narrow QRS
• Delta wave absent
• Down through AV node
• Up through accessory pathway

• Antidromic
• Wide QRS
• Delta wave present
• Down through accessory pathway
• Up through AV node

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Tachydysrhythmias

• WPW
• Treatment
• Stable vs Unstable
• Depends on 3 observations
• Symptoms of instability
• QRS duration or Delta wave presence
• QRS regularity or irregularity
• Regular Orthodromic
• Most common
• Treat same as SVT
• Regular Antidromic or any irregular rhythm
• High risk of Vfib (esp when RR interval lt 0.20)
• Avoid AV nodal blocking drugs (CCB, BB, dig,
  adenosine)
• Procainamide is drug of choice or cardioversion
  if gt 250 bpm
• Amiodarone can also be considered

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Tachydysrhythmias

• Wide Complex Tachycardias
• gt 100 bpm and QRS gt 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

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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

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Distinguishing VT from SVT with aberrancy

• VT accounts for 80 of all cases of regular
  wide-complex 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.

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Tachydysrhythmias

• Ventricular Tachycardia
• gt 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 gt 0.14 sec
• Extreme LAD
• No response to vagal maneuvers
• V1 R, qR or RS
• V6 S, rS, or qR

• SVT with Aberrancy
• lt 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 lt 0.14 (usually)
• Normal Axis
• Vagal maneuvers
• V1 rsR
• V6 qRs

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A-V Dissociation, Fusion, and Capture Beats in VT
V1
E
F
C
ECTOPY
FUSION
CAPTURE
Fisch C. Electrocardiography of Arrhythmias.
1990134.
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Tachydysrhythmias

• Brugada Criteria

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Tachydysrhythmias

• Morphology Criteria in leads V1 and V6

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The Brugada Criteria
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Morphology Criteria for VT
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Tachydysrhythmias

• Brugada P, et al A new approach to the
  differential diagnosis of regular tachycardia
  with wide QRS complex. Circulation 831649. 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.

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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

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Tachydysrhythmias
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Tachydysrhythmias

• Ventricular Tachycardias
• VTach
• Monomorphic
• Polymorphic
• Vfib/flutter

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Tachydysrhythmias

• Monomorphic VTach
• Consistent QRS complexes
• Seen in CAD/IHD, lytes abnormalities, hypoxemia
• Tx stable
• Lidocaine
• Cardioversion
• Procainamide, Amio, Magnesium

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Tachydysrhythmias

• Case 5
• 80 yr old female feeling weak and dizzy, EMS
  patch in rhythm strip because unsure

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Tachydysrhythmias
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Tachydysrhythmias

• Polymorphic Vtach
• QRS of varying morphology
• More severe disease
• Torsades de Pointes
• Clinical Criteria
• Ventricular rate gt 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

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Tachydysrhythmias

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

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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

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