Normal Rhythms, Enlargement Patterns And Conduction Disturbances Flashcards
Sinus arrhythmias
Dogs only
Wondering pacemaker
Vagally mediated
Changes in P wave height
Taller P waves with faster heart rates and higher sympathetic tone
Shorter P waves with slower heart rates and higher vagal tone
RA enlargement
Tall, peaked P waves in leads II III and avF
LA enlargment
Wide, sometimes notched P waves
LV enlargement
Tall R waves in lads I II III and avF
Or
Wide QRS
Sinus rhythm
Upright P in I II III and avF
RV enlargement
Deep S waves in leads I II III and avF
Dogs with tricuspid valve dysplasia can also have ‘splintered’ QRS complexes (also referred to a Rr pattern)
Hyperkalemia
Mild - spiked tall T wave
Moderate - small P wave, tall T waves, bradycardia
Severe - less of P waves, bradycardia, wide QRS complexes, right bundle branch block
Hypokalemia and hypocalcemia
Could cause QT interval prolongation
Pericardial effusion
Complex size reduced due to attenuation by the fluid or because of reduced intra cardiac blood volume
Electrical alternans = beat to beat QRS variation
Due to swinging of the heart within the pericardium
Right bundle branch block (RBBB) ECG hallmark
Widened QRS (>80 ms dog)
RBBB
+/- underlying cardiac disease
1st degree AV block
Slow AV node conduction
But all impulse get through
Prolonged PR interval
Etiologies for 1st degree AV block
Structural AV node disease Elevated vagal tone Drugs Hyperkalemia Hypothermia
2nd degree AV block
Some sinus depolarizations get through others don’t
Can also be due to elevated vagal tone
Diseases that increase vagal tone can cause
GI disease, ocular disease, respiratory disease, urinary tract disease
Types of 2nd degree AV block
Mobitz type I (Wenkeback phenomenon)
Mobitz type II
High grade
Mobitz type I
Wenkeback phenomenon
Progressive PR prolongation prior to block
May be due to elevated vagal tone or drugs can be normal in athletic horses and very young puppies
Treatment for Mobitz type I
Vagalytics
Sympathomimetics
Discontinue drugs
Mobitz type II
No PR prolongation prior to block
Usually indicates structural cardiac disease
Less common than Mobitz type I
Monitor
High grade
Cannot determine if Mobitz type I or II because there are no 2 consecutively conducted beats
Describes by the ratio of. P waves. To QRS complexes
Usually associated with structural AV node disease (no or minimal response to atropine)
If non atropine can responsive and clinical signs present, pacemaker implantation is indicative
3rd degree AV block
No sinus depolarizations get through
SA node continues to depolarize fast
Escape rhythms take over to “rescue” the ventricles
No relationship between P and QRS (no constant PR)
Slow ventricular rate (depends on level of escape)
Escape rhythms for 3rd degree AV block
Junctions escape rhythm
Ventricular escape rhythm
Junction all escape rhythm
40 - 60 bpm
Complexes look “supraventricular”
Ventricular escape rhythm
20-40 bpm
Complexes look “ventricular”
Etiologies from 3rd degree AV block
Idiopathic (probably degenerative) Infectious/inflammatory rarely congenital Rarely neoplastic Associated with hyperthyroidism and cardiomyopathy in cats
Treatment for 3rd degree AV block
Pacemaker implantation
Low voltage complexes
Normal variations Obesity Pleural effusion Pericardial effusion Hypothyroidism Pneumothorax Pulmonary thromboembolism Hypoproteinemia
