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Cardiology

 101:  All  you  need  to  know  


VETgirl…On-­‐The-­‐Run  
about  interpre7ng  ECGs  
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Marc  S.  Kraus,  DVM  


Dip  ACVIM  (Cardiology,  Internal  Medicine)  
Dip  ECVIM-­‐CA  (Cardiology)  

Introduction Introduction
Garret Pachtinger,
VMD, DACVECC Jus7ne  A.  Lee,  DVM,  
DACVECC,  DABT  
COO, VETgirl CEO,  VETgirl  

Conflict of Interest Disclosure


Introduction

Marc  Kraus,  DVM,  


DACVIM,  ECVIM          

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Introduction Objec7ves  
•  Why  perform  an  ECG?  
Marc  Kraus,  DVM,  
DACVIM,  ECVIM           •  Best  way  to  interpret  ECGs  
–  Calculate  heart  rate  
–  Chamber  enlargements  
•  Treatment  
–  Supraventricular  arrhythmias  
–  Ventricular  arrhythmias  
–  Brady-­‐arrhythmias  

Indica7ons  for  ECG  Recordings   Indica7ons  for  ECG  Recordings  


•  Arrhythmias  and  heart  rate  disturbances     •  Assessing  changes  in  ECG  morphology  and  
 detected  on  auscultaFon   heart  rate  due  to:  
•   History  of  syncope  (fainFng)  or  episodic   –  electrolyte  imbalances  associated  with  
 weakness   extracardiac  disease  or  drug  toxiciFes.  
•  Cardiac  monitoring  during  anesthesia   •  ECG  may  also  be  helpful  to  idenFfy  anatomical  
•  Cardiac  monitoring  in  criFcally  ill  paFents   changes  due  to:  
–   myocardial  hypertrophy  or  dilaFon,  
•  Monitoring  changes  in  rate  and  rhythm  due  to  
–   and  detect  pericardial  disease.    
drug  administraFon  

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Genera7on of the PQRST
Systema7c  Approach  to  ECGs  
•  Is  there  a  P  wave  for  every  QRS  complex?  
•  The  relaFonship  of  the  P  wave  and  QRS  
complexes  
–  Is  there  a  P  wave  in  front  of    every  QRS  complex  
–  Is  there  a  QRS  complex  following    every  P  wave?      
•  Are  the  QRS  complexes:  
–  Supraventricular  or  
–  Ventricular  

Determining  Heart  Rate  


What  is  the  heart  rate?  

50mm/s 10mm/mV

•  BIC pen is 15cm = 150 mm (30 large squares) = 3 sec


•  3 sec: if paper speed is 50mm/s

•  Average HR = 5 beats/3 sec = 5 x 20 = 100 bpm

Ventricular Enlargement Bundle Branch Blocks

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6  limb  leads  together  form  the   Right  Bundle  Branch  Block  
hexaxial  lead  system  of  the  
frontal  plane    

Normal  ECG  amplitudes  and   Rhythm  Analysis  


dura7ons  in  the  dog  and  cat   Sinus

DOG CAT
Normal conduction Abnormal conduction
Heart  rate   Puppy:70-­‐220   120-­‐240bpm    
Adult:  70-­‐180  
P  wave  Amplitude   Max:  0.4mV   Max  :  0.2mV  
Normal rate Abnormal rate Bundle branch blocks Sick sinus
P  wave  DuraFon   Max  0.04s   Max  :  0.04s     Left/Right syndrome

PR  interval   0.06-­‐0.13s   0.05-­‐0.09s     Bradycardia Tachycardia AV blocks


1st
QRS    amplitude   Max:  2.5mV  small  breeds   Max:  0.9mV  
2nd
                 3.0  mV,  large  breeds   Regular rhythm Irregular rhythm 3rd
QRS  duraFon   0.06s   0.04s    
Electrical  axis   +40°  to+100°     0  to+160°    
Sinus rhythm Sinus arrhythmia Not sinus

Image copyright Marc Kraus© SVT VT

Ventricular  Tachycardia  Algorithm   Charles,  Poodle  11  y    


chronic  mitral  insufficiency  and  coughing  
Ventricular tachycardia (VT)

Ectopic  focus  is  firing  from  the  atria  or  within  the  AV  node:    
•  Atrial  premature  (ectopic)  complex    (APC)  
Rapid VT (160-380 bpm) “Slow” VT (40-150 bpm) –  QRS  complex  looks  90%  like  a  normal  beat  
–  P’  (arrow)  wave  may  be  buried  in  preceding  T  wave,  could  
be  upright  or  negaFve  (any  morphology)    
Idioventricular P - P’ P - P’ P - P
Polymorphic VT
rhythm or accelerated
Monomorphic VT Image copyright Marc Kraus©
ventricular rhythm

Supraventricular Ventricular escape


tachycardia with rhythm
bundle branch block (3rd AV block)

Image copyright Marc Kraus©

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First  and  Second  Degree  AVB   What  is  this?  
I

II ? ? ?
200 220 200 240

Image copyright Marc Kraus©

III

50 mm/sec

Second degree AV block (Mobitz type 1)


•  ?= blocked P waves
•  PR interval gets progressively longer until block occurs

Sick  Sinus  Syndrome   Bradyarrhythmias  Therapy  


 brady-­‐tachy    
•  Sick  Sinus  Syndrome  
–  SympathomimeFc  drugs:  Terbutaline  
–  Or:  (parasympatholyFc  drugs:  Propantheline)  
–  Usually  end  up  with:  Pacemaker  

•  AV  block  (3rd  or  high  grade  2nd)  


–  Pacemaker  
–  !Atropine  cannot  work!  May  worsen  HR  

Atrial  fibrilla7on  with  a  LBBB  


Ventricular  Tachycardia  

Fig K

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Atrial  Tachycardia  
Bradycardia-­‐associated  syncope  in  boxers  
variable  AV  conduc7on  
with  ventricular  tachycardia  

Bradycardia-­‐associated  syncope  in  boxers   Atrioventricular  Block,  


with  ventricular  tachycardia   ventricular  bigeminy  

Bradycardia-­‐associated  syncope  in  seven  boxers  with  ventricular  


tachycardia  (2002-­‐2005).  JVIM  2008,  Thomason,  Kraus,  Calvert  

Are  these  VPCs?   What  is  this?  

Ventricular tachycardia
? ? ?
Fusion beat
VPC VPC VPC VPC
Image copyright Marc Kraus©

P P P P P? P

Image copyright Marc Kraus©

25 mm/s 5 mm/mV
Third degree AV block:
•  No P waves are associated wit the QRS
•  QRS wide and bizarre: ventricular escape beat (NOT premature, but late beats)
•  HR of escape rhythm very slow : 30 bpm
•  Tx: pacemaker

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Does  this  need  treatment?  
Is  this  scary?   What  is  the  rate?    

50mm/s, 10 mm/mV

Polymorphic VT at 550 bpm; risk to degenerate into ventricular fibrillation Monomorphic ventricular tachycardia: RR interval =10 mm; 3000/10= 300 bpm
Yes – needs antiarrhythmic treatment !

Does  this  need  treatment?   Is  this  also  slow  VT?  

P P P
VPC VPC

Image copyright Marc Kraus© Image copyright Marc Kraus©

440 440
460 460

50mm/s 10mm/mV

Slow  VT  or  isorhythmic  dissocia7on:  usually  no  tx  


25 mm/s 10mm/mV Sinus rhythm with left bundle branch block (mimicking VT)
•  Sinus  rhythm  and  VT  have  the  similar  slow  HR  (75  bpm)     •  P waves before every QRS
•  When  sinus  rhythm  slows  down,  VT  takes  over   •  QRS wide and bizarre: conduction disturbance

What  is  the  blood  pressure  during  B?  


What  is  going  on  here?  
APC   VPC  

Ventricular fibrillation

APC:  normal  QRS,  premature  


VPC:    wide  and  bizarre,  premature,  QRS  complex  not  preceded  by  P  

•  Blood  pressure    is  0  during  V  fib!  


Ventricular  bigeminy  (every  VPC  coupled  to  a  normal  beat)   •  MUST  defibrillate  

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Treatment  of  ventricular  tachycardia  
If  lidocaine  does  not  work  for  life  –threatening  VT!  
•  Goal:    
•  Ask  yourself  is  it  really  VT?    
–  Reduce  risk  of  sudden  death  
–  Reduce  symptoms:  syncope,  episodic  weakness   –  Ddx:  SVT  with  a  bundle  branch  block  paqern  

•  How?     •  Did  the  VT  slow  down  aler  Lido?  


Reduce/  abolish  the  arrhythmia:   –  Improves  cardiac  output:  VT  beqer  tolerated  
–  Slow  the  rate  of  VF  so  it  is  hemodynamically  beqer  tolerated   –  Does  the  animal  feel  beqer  (blood  pressure)?  
–  Shorten  the  duraFon  of  episodes  of  VT  
•  If  not:  replace  lido  with  Procainamide:    
–  5  to  15  mg/kg  IV  bolus  
•  In  deciding  on  treatment:  Differen7ate   –  Slow  infusion  over  10  min  
between:   –  Followed  by  CRI:  25  to  50  ug/kg/min  
–  Side  effects:  
–   “fast”  VT  (170-­‐  350  bpm)    
–  hypotension et neg inotrope
–   “slow”  VT  (80  to  160  bpm)    
–  or  combine  Lido  with  IV  beta  blockers  or  oral  sotalol  

VT  caused  by  increased  concentra7ons  of   Stable,  but  dangerous  VT    


catecholamines:  Beta-­‐blockers     Oral  an7arrhythmic  therapy  

•  VT  during  a  cath  procedure:  Valvuloplasty   Sotalol  (2  to  3  mg/kg  PO  q  12h)  
•  Thyroid  storm  (cat)  
•  Combined  beta  blocker  with  K  channel  blocker  
•  Esmolol  IV:   •  efficacious  in  most  Boxers  (Meurs  et  al.  JAVMA  2002)      
–  50  -­‐  100  µg/kg  IV  bolus  (max  500  µg/kg)   •  pro-­‐arrhythmic  effects  as  monotherapy  in  German  
–  CRI  at  50-­‐200  µg/kg/min  (costly!)  
shepherds  (Gelzer  et  al    JVC  2010)    
–  CombinaFon  of  esmolol  with  lidocaine  
–  If  esmolol  is  combined  with  procainamide:   •  Dobermans:  If  severe  systolic      
•  Severe reduction in cardiac output  dysfuncFon:  
–  FracFonal  shortening<15%  
•  Propranolol:    beta-­‐blocking  effects  of  sotalol  may      
–  Dog  &  cat:  0.01-­‐0.1  mg/kg  slow  IV  bolus      be  too  negaFve  inotrope  

Stable,  but  dangerous  VT  AlternaFve  


oral  therapies     Refractory  VT  

•  In  dogs  with  severe  systolic  dysfunc7on     •  Amiodarone  PO  


–  mexileFne  (4  to  8  mg/kg  q  8h)     –  10  mg/kg  q  12h  for  1  week  (loading  dose)  
   plus   –  then  5  mg/kg  q  24h  (maintenance)  
–  atenolol  (0.5  to  2  mg/kg  q  12-­‐24h)  
•  Titrate  up  as  tolerated     •  Risk  of  side  effects  (hepatopathies)  
–  anorexia,  vomiFng,  lethargy  
•  Severe,  refractory  VT  or  recurrent  fain7ng     –  elevaFon  of  liver  enzymes  (Doberman!)  
–  CombinaFon  of  sotalol  with  mexileFne  (use   –  Check  liver  enzymes  every  2  months    
regular  dosages  of  each)   –  Liver  toxicity  is  reversible  

(Meurs KM et al. 2003)


Kraus MS et al JVIM 2009

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What  is  missing?   Electrical  Alternans  

Alternating amplitude of
QRS complexes
Atrial  standsFll  with  slow  juncFonal  rhythm:  50  bpm  
•  No  P  waves      
•  QRS  narrow  
•  Atrial  pathology  or  hyperkalemia  

Common  SVA’s   Atrial  Fibrilla7on  

•  AV  node  independent  rhythms    


–  sinus  node  tachycardia  
–  atrial  fibrilla7on  
–  atrial  flu^er  
–  ectopic  atrial  tachycardia  
•  AV  node  dependent  SVA’s  
–  AV  nodal  reentrant  tachycardia  
–  atrioventricular  reentrant  tachycardia    
•  (bypass  tract-­‐mediated)  

Atrial  Fibrilla7on    
Is  this  atrial  fibrilla7on?  

•  Rhythm too regular for atrial fibrillation


•  Artifact mimicking AF: Purring or 60 cycles (grounding, check filters)

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What  is  this  rhythm?   Atrial  Fibrilla7on  (AF)  
What  is  this  species?  
•  AF  is  the  most  common  SVTarrhythmia  
•  Atrial  enlargement    
–  secondary  cardiomyopathy  
–  volume  overload  (CVD,  DCM,  PDA,  VSD)  

•  AF  without  apparent  underlying  heart  disease  


–  idiopathic  or  “lone”  AF,    
–  “lone”  AF  can  progress  over  Fme  
•  Irregularly irregular rhythm
•  No P waves but fine F waves
•  Small QRS
•  Feline A fib

Rate  Control  
Treatment  of  AF  
Rate  control    vs  conversion  
Doberman  with  AF  and  DCM  

Before  
•  Rate  control  =  slowing  of  ventricular  response   Treatment:    
HR  225  bpm!  
– If  significant  cardiac  pathology  (and  CHF)  
– If  the  average  heart  rate  by  24h  Holter  is  >  140  bpm  
– Cats  with  AF   Treatment:    
Digoxin  alone  
•  Conversion  to  sinus  rhythm   HR  180  bpm!  
– VERY  difficult  to  achieve  and  maintain  
– Giant  breed  dog  with  no  or  minimal  cardiac  abnormaliFes   Digoxin  and  
DilFazem  
– Recent  onset  AF     HR  100  bpm!  

– AF  induced  during  anesthesia  or  by  catheterizaFon  


CombinaFon  drug  therapy  DIGOXIN  +  DILTIAZEM    
is  more  effecFve  than  monotherapy  

Atrial  Tachycardia  
Conversion  to  sinus  rhythm  (lone  AF)   variable  AV  conduc7on  
•  DC  cardioversion  :  
–  “Synchronizing”  defibrillator  
required  
–  General  anesthesia    
–  Risk  of  recurrence  of  AF    
•  Amiodarone:  
–  Loading  dose  for  7-­‐10days:  400  
mg  SID  
–  Maintenance  :  200  mg/kg  SID  
–  success  rate??  

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Atrial  flu^er  AFL  
Atrial  Flu^er  
•  ECG  characterisFcs:  
•  Reentry  circuit   –  regular  saw  tooth  shaped  undulaFon  
•  Loop  is  typically  in   –  rapid,  ventricular  response  
counter  clockwise   –  rapid  rhythm,  but  conducFon  can  be  variable  
direcFon  (humans)  
–  Rarely,  1:1  AV  conducFon  can  occur  and  may  be  
•  Loop  consists:   lethal.  
–  Tricuspid  valve  annulus  
–  Atrial  septum  
–  Crista  terminalis  

Courtesy Blaufuss
medical

WPW  
Preexcita7on  during  sinus  rhythm  
•  Short  PR  interval  (40ms)   •  Terminal  forces  of  V1  nega7ve:  
•  Delta  wave   suspected  loca7on  of  pathway:  RA-­‐RV  
•  Wolf  Parkinson  White  
Syndrome  

Delta wave

PR

WPW   WPW  iniFaFon  

Blaufuss medical

QUESTIONS  ?  
Thank you to!
•  For ECG images:
Dr. Anna Gelzer,
DACVIM
(Cardiology),
ECVIM
(Cardiology)

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Dr. Garret Pachtinger


•  WVC, March 2016

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