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Cardiology Quarterly Radiograph of Heart Sound Cardiology Contact About
Cardiology
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Concepts Cases the Month of the Month Database
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CLINICAL CARDIOLOGY CONCEPTS
for the dog and cat
Michael R. O'Grady, DVM, MSc, Diplomate ACVIM (Cardiology)
M. Lynne O'Sullivan, DVM, DVSc, Diplomate ACVIM (Cardiology)
Contents

General
1 What is a P wave? What electrocardiographic event does this represent?
The P wave is the electrocardiographic representation of electrical activation of the atrial myocardium.
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P amp = amplitude of the P wave; P dur = duration of the P wave; PR int = PR interval; R amp = amplitude of the R
wave; QRS dur = duration of the QRS complex; QT int = QT interval; T amp = amplitude of the T wave.
The amplitude measurement of the P wave depends on the calibration pulse (how many mm = 1 mv).
The duration measurement of the P wave depends on the paper speed (how many msec = 1 mm).
top : General
2 What is the PR interval? What is the significance of the PR interval?
The PR interval is the electrocardiographic representation of the delay in electrical activation of the ventricles after
sinoatrial nodal discharge. This interval is mainly a result of slow conduction through the atrioventricular node.
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The duration measurement of the PR interval depends on the paper speed (how many msec = 1 mm).
top : General
3 What is the significance of the QRS complex? How are a Q, R, S, and QS
different?
The QRS complex is the electrocardiographic expression of the electrical activation of the ventricular myocardium.
For a wave to be defined as a Q wave it must fulfill the following criteria:
a. It must be a negative deflection.
b. It must be the first deflection of the QRS complex.
c. It must be followed by an R wave.
Thus there can be only one Q wave per QRS complex.
For a wave to be defined as an R wave it must fulfill the following criteria:
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a. It must be a positive deflection.
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b. All positive deflections are R waves and only R waves (within the QRS complex).
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There can be several R waves per QRS complex.
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For a wave to be defined as an S wave it must fulfill the following criteria:
b. It must follow an R wave.
There can be several S waves per QRS complex.
For a wave to be defined as a QS wave it must fulfill the following criteria:
b. There must be no R wave in the QRS complex.
Therefore it describes a QRS complex with only one deflection and this deflection is negative.
Comment: It should be noted that a QRS complex may thus consist of only an R wave, or only of RS waves, or only
of QR waves, etc.
top : General
4 What is a T wave? What is the significance of a T wave?
The T wave is the electrocardiographic expression of repolarization of the ventricular myocardium.
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For any deflection on an electrocardiogram to be considered as a "beat" it must have a repolarization wave (T
wave).
In domestic animals, patient cooperation is usually poor and therefore movement artifact is frequently encountered
on the electrocardiogram. These deflections can usually be diagnosed as artifact as opposed to a QRS complex
because of the absence of a T wave.
top : General
5 What is the significance of a positive deflection in a lead? Of a negative
deflection in a lead?
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An electrical lead used to examine the heart on the ECG can be described in terms of a negative pole and a
positive pole.
As a wave of electrical depolarization moves parallel to the direction of a lead, if it moves towards the positive pole
of the lead, a positive deflection occurs on the ECG. If it moves toward the negative pole of the lead, a negative
deflection occurs on the ECG.
top : General
6 What is the frontal plane diagram? What are the horizontal plane leads?
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The frontal, left sagittal, and transverse (also called horizontal) planes are illustrated in the cat. Leads I, II, III, aVR,
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aVL, and aVF are frontal plane leads. Leads V1, V2, V3, V4, V5, V6, and V10 are horizontal (or transverse) plane
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leads.
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In the illustration, a crosssection of the heart is superimposed on the frontal plane diagram.
The arrow heads point toward the positive pole of each lead.
The frontal plane diagram shows the relationship of the 6 leads in the frontal plane. This diagram includes the
angles in the frontal plane and the direction of each lead with its negative and positive pole.
The frontal plane corresponds to the radiographic V/D or D/V view of the heart.
Transverse Section At The 6th Intercostal Space Showing The Position Of The Horizontal Plane (Precordial)
Leads:
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The precordial leads (horizontal plane leads) are often the most useful leads to identify the presence of P waves.
The identification of P waves is the most crucial step in the identification of most dysrhythmias as will be discussed
later.
top : General
7 What is the significance of the MEA of the QRS complex?
The mean electrical axis (MEA) of the QRS complex is usually determined in the frontal plane. This represents the
direction (expressed in degrees) of the net or average direction of activation of the entire ventricular myocardium.
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There are three common methods of calculating the MEA in the frontal plane. All of these are merely
approximations. Individuals should use whichever method they feel comfortable with.
a. The Vector Method: Using leads I, II or III and the frontal plane diagram, calculate the algebraic sum of the
QRS deflections in any two leads (this does not include the P wave or the T wave). Let us for example
consider using the complexes of leads I and III. Plot the algebraic sum of lead I on its axis on the frontal
plane diagram. Similarly plot the algebraic sum of the QRS complex of lead III on its axis on the frontal plane
diagram. Draw lines perpendicular to the their respective axes at the points plotted on the lead axes I and III.
Note the point of intersection of these two perpendicular lines. A line drawn from this intersect to the center
of the diagram describes the MEA. See the example below:
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b. The Isoelectric Method: Find the lead, of the 6 leads in the frontal plane, that is the most isoelectric (the
algebraic sum of all the deflections of the QRS in that lead comes closest to zero) (again omit the T wave).
Next, find the lead on the frontal plane diagram that is perpendicular to this isoelectric lead (the MEA will lie
along this perpendicular lead). Note the net polarity of the complexes in this perpendicular lead. If the net
polarity of these complexes is positive, the MEA is toward the positive pole of the perpendicular lead; if the
net polarity of these complexes is negative, the MEA is toward the negative pole of the perpendicular lead.
c. The Largest Net Deflection Method: Find the lead, of the 6 leads in the frontal plane, that contains the QRS
complex with the largest net deflection (the algebraic sum of all the deflections of the QRS in that lead is the
largest value [positive or negative]). The MEA will lie along this lead. If this largest net deflection is positive,
the MEA is toward the positive pole of this lead with the largest net deflection; if this largest net deflection is
negative, the MEA is toward the negative pole of this lead with the largest net deflection.
top : General
8 Why should I bother determining the MEA?
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Determining the MEA is very useful to identify right ventricular enlargement. A MEA of 100 to 75 degrees in the dog
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or 160 to 75 degrees in the cat suggests right ventricular enlargement.
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The MEA also helps determine the nature of aberrant conduction disturbances (so called bundle branch block).
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top : General
9 What is a sinus rhythm?
A sinus rhythm is a rhythm which originates in and is controlled by the sinoatrial node. This rhythm is the normal
cardiac rhythm in all domestic animals. To determine if a rhythm is sinus or not based on the ECG requires the
following criteria:
1. There is a P wave for every QRS complex.
2. The PR interval is relatively constant (especially if the R wave to R wave interval varies).
3. The P wave is positive in lead II.
Comments: In that the P wave doesn't indicate sinoatrial activation but the result of sinoatrial activation, we can
only infer the normalcy of sinoatrial activity from the routine ECG.
top : General
10 What is a sinus arrhythmia?
A sinus arrhythmia is an irregular ventricular rhythm which is of sinoatrial origin. On the ECG, the QRS to QRS
interval varies and there is a P wave for every QRS complex.
Example 1: Sinus Arrhythmia and Wandering Atrial Pacemaker in the Dog
Etiology:
most cases of sinus arrhythmia are phasic and associated with respiration
the rate increases with inspiration and decreases with expiration
associated with relatively slow rates
the sinus arrhythmia of respiratory origin occurs due to the influence of vagal tone
Individuals with respiratory disease tend to have augmented sinus arrhythmia.
Consequences:
This is a normal finding particularly in fit individuals. An irregular cardiac rhythm may have been detected on
an individual during physical examination. The finding of sinus arrhythmia on ECG confirms the presence of
an arrhythmia but also establishes that this irregularity is non pathologic.
It is important to distinguish this rhythm from that of atrial premature contractions.
Treatment:
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none required
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Example 2: Sinus Arrhythmia and Wandering Atrial Pacemaker in the Dog
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10 fine lines vertically = 1mV; 25 fine lines horizontally = 1 sec
top : General
11 What is a wandering atrial pacemaker?
ECG Findings:
variable amplitude and/or morphology of the P wave
the change in P wave amplitude and / or morphology tends to gradually shift from normalcy
associated with sinus arrhythmia
the heart rate is in the mid to low normal range
Example of Wandering Atrial Pacemaker in the Dog Put cursor over image for more information
10 fine lines vertically = 1 mV; 25 fine lines horizontally = 1 second
Etiology:
associated with increased respiratory effort
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usually a normal finding
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occurs due to increased vagal tone
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Consequences:
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normal
usually occurs in association with sinus arrhythmia
in the face of a marked sinus arrhythmia, altered P wave morphology can be misinterpreted as atrial
premature beats
Treatment:
none required
Further Examples:
Wandering Atrial Pacemaker example 1 (highlighted hints)
Wandering Atrial Pacemaker example 2 (highlighted hints)
Chamber Enlargement
top : Chamber Enlargement
12 Approach to the ECG to determine chamber enlargement
1. Determine the ventricular rate note paper speed.
2. Determine the atrial rate note paper speed.
3. To assess atrial enlargement:
measure P wave duration in lead II note paper speed
measure P wave amplitude in lead II note calibration
4. To assess ventricular enlargement:
measure QRS duration in lead II note paper speed
measure R wave amplitude in lead II note calibration
examine for S waves in leads I, II, III
examine and measure S wave amplitude in lead V3 note calibration
determine MEA in frontal plane
examine ST segment in lead II
13 What is the significance of a P wave that is too tall or too wide?
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Normal Too Tall Too Wide
a. An electrocardiographic criterion of left atrial enlargement is a P wave that is too wide in lead II.
dog: P > 0.04 sec
cat: P > 0.04 sec
b. An electrocardiographic criterion of right atrial enlargement is a P wave that is too tall in lead II.
dog: P > 0.4 mv
cat: P > 0.2 mv
c. An electrocardiographic criterion of biatrial enlargement is a P wave that is too tall and too wide in lead II.
Comments:
in the presence of a wandering pacemaker, it is inappropriate to measure P wave amplitude (just omit this
measurement)
all measurements are made in lead II, usually at 50 mm/sec paper speed
the sensitivity and specificity of the ECG criteria for atrial enlargement are low
14 What are the electrocardiographic criteria of left ventricular enlargement?
a. Dog:
R amplitude in Lead II
<20kg: R amplitude > 2.5 mv
>20kg: R amplitude > 3.0 mv
b. Cat:
R amplitude in Lead II > 0.9 mv
Example of Left Ventricular Enlargement in the Dog Place cursor on picture for more information
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Further Examples:
Left Ventricular Enlargement example 1 (highlighted hints)
Left Ventricular Enlargement example 2 (highlighted hints)
15 What are the electrocardiographic criteria of left ventricular concentric
hypertrophy?
It is our experience that the ECG is usually completely normal in cases of left ventricular concentric
hypertrophy
Tilley and others suggest that a shift in the MEA to the left occurs in this disorder. This has not been
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substantiated.
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The R wave amplitude in lead II may be increased.
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The QRS duration in lead II may be increased.
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16 What is the electrocardiographic evidence of right ventricular enlargement?
Dog:
1. Presence of an S wave in leads I, II, III.
2. MEA in the frontal plane shifted to the right (pointing to the right ventricle): 100o to 75o
3. Deep S wave in lead V3; S >= 0.7 mv
4. S>R in lead V3
if all 4 criteria are present, there is strong evidence of right ventricular enlargement
the presence of any 2 criteria is still very good evidence of right ventricular enlargement
even the presence of 1 criteria is strongly suggestive of right ventricular enlargement
Comments:
V3 is a horizontal plane lead. It is useful to help detect right ventricular enlargement. At times the frontal plane may
show QRS complexes that are isoelectric in all 6 leads. In such cases a V3 trace is helpful as the criteria for right
ventricular enlargement may only be present in V3.
Transverse Section At The 6th Intercostal Space
Showing The Position Of The Horizontal Plane Leads
Cat: MEA in the frontal plane shifted to the right (points to the right ventricle): 160 to 75
Example of Right Ventricular Enlargement in the Dog
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Further Examples:
Right Ventricular Enlargement example 1 (highlighted hints)
Normal ECG Parameters
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top : Normal ECG Parameters
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17 Normal ECG Diagram
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I. Diagram of Normal ECG with Location of Routine Measurements
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P amp = amplitude of the P wave; P dur = duration of the P wave; PR int = PR interval; R amp = amplitude of the R
wave; QRS dur = duration of the QRS complex; QT int = QT interval; T amp = amplitude of the T wave.
top : Normal ECG Parameters
18 Normal Small Animal Electrocardiographic Parameters
Normal Electrocardiographic Parameters in the Dog and Cat
Parameter Canine Feline
Adults: 70160
Heart Rate (beats per minute) Toy Breeds: up to 180 160240
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Puppies: up to 220
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Normal sinus rhythm
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Normal sinus rhythm
Rhythm Sinus arrhythmia
Sinus tachycardia
Wandering atrial pacemaker
Intervals (seconds)
P < 0.04 < 0.04
PR 0.06 to 0.13 0.05 to 0.09
< 20 kg: < 0.05
QRS > 20 kg: < 0.06 < 0.04
Giant breeds: < 0.065
QT 0.15 to 0.25 0.12 to 0.18
Parameter Canine Feline
Amplitudes (mV) in lead II
P < 0.4 < 0.2
< 20 kg: < 2.5
R < 0.9
> 20 kg: < 3.0
MEA +40 to +100 5 to +160
Criteria for Chamber Enlargement: Summary
Chambers: ECG Parameter: Body Wt Canine Feline
Left Atrium PII duration > 0.04 s > 0.04 s

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Right Atrium PII amplitude >0.4 mv >0.2 mv
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<20 kg >2.5 mv
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Left Ventricle RII amplitude >0.9 mv w
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>20 kg >3.0 mv
Pattern of SI, SII, & SIII Present
MEA points to Rt Vent Present Present
Right Ventricle
S in V3 >0.7 mv
S in V3 > R in V3 Present
Dysrhythmias
top : Dysrhythmias
19 Approach to the ECG to assess dysrhythmias.
Try the diagnostic algorithm here (a chart form is here).
1. Determine the ventricular rate note paper speed.
2. Determine the atrial rate note paper speed.
3. Are P and QRS associated?
same rate
reasonable PR interval
consistent PR interval
4. Determine PR interval note paper speed
does it vary?
5. Are there any P waves that are not followed by a QRS complex?
6. Are there any QRS complexes with no P waves?
7. Determine the width of the QRS complexes note paper speed.
8. Is the rhythm regular or irregular?
9. Any premature beats? note morphology and duration
10. Are the P waves positive in lead II?
11. Are the QRS complexes of normal morphology?
The critical feature with most dysrhythmias is to find the P waves (if present); note if the atrial rate is equal to, less
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than, or greater than the ventricular rate, and note if there is any relationship between the P waves and the QRS
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complexes.
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Dysrhythmias Algorithm to Diagnose Cardiac Rhythm Disorders By Electrocardiography
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DO QRS
COMPLEXES
HEART P WAVES
RHYTHM HAVE DISORDERS
RATE PRESENT?
ASSOCIATED
P WAVES?
Sinus Bradycardia
YES
YES 2nd Degree Heart Block
SLOW NO 3rd Degree Heart Block
Hyperkalemia
NO
Persistent Atrial Standstill
Normal Sinus Rhythm
YES
NORMAL Atrial Flutter
NO Ventricular Tachycardia
Hyperkalemia
REGULAR NO
Persistent Atrial Standstill
Sinus Tachycardia
Supraventricular
YES
Tachycardia
YES Atrial Flutter
Ventricular Tachycardia
FAST
NO NonParoxysmal Junctional
Tachycardia
Supraventricular
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Tachycardia (P waves
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NO
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present but buried in QRS
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DO QRS
COMPLEXES
HEART P WAVES
RHYTHM HAVE DISORDERS
RATE PRESENT?
ASSOCIATED
P WAVES?
Sinus Bradycardia
Sinus Arrhythmia
YES
YES Sick Sinus Syndrome
SLOW
2nd Degree Heart Block
NO
NO Slow Atrial Fibrillation
Sinus Arrhythmia
YES
NORMAL Atrial Flutter
IRREGULAR Ventricular Tachycardia
NO
(rhythm is usually regular)
NO Atrial Fibrillation
Sinus Tachycardia
Atrial Flutter
YES
Supraventricular
YES Tachycardia
FAST Ventricular Tachycardia
(rhythm is usually regular)
NO
Nonparoxysmal Junctional
Tachycardia
Atrial Fibrillation
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NO Atrial Fibrillation F-
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Bradycardias
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top : Bradycardias
20 What is bradycardia?
Bradycardia is present when the ventricular rate is too slow:
dog (< 20 kg) = < 70 bpm
dog (> 20 kg) = < 60 bpm
cat = < 100 bpm
top : Bradycardias
21 What is sinus bradycardia?
This refers to a sinus rhythm wherein the sinoatrial rate is bradycardic.
Example of Sinus Bradycardia in the Dog
Etiology:
1. Enhanced parasympathetic tone as with:
Increased respiratory effort as with respiratory disease.
Gastric irritation.
Increased CSF pressure.
2. Hypothyroidism
3. Hypothermia
4. Hyperkalemia
5. Hypoglycemia
6. Drug therapy
Consequence:
1. profound bradycardia will cause weakness, hypotension, syncope
Therapy:
1. Treat the underlying cause of the bradycardia
2. Atropine may abolish the bradycardia (atropine 0.04 mg/kg IV)
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top : Bradycardias
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22 What is heart block?
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Heart block refers to a group of disorders characterized by variable conduction from the atria to the ventricles. c u -tr a c k
Heart block can be classified as
1st degree Heart Block prolonged conduction across the atrioventricular node
2nd degree Heart Block failure of SA impulse to activate the ventricular myocardium
3rd degree Heart Block no conduction through AV node, ventricular activation due to an automatic
ventricular pacemaker focus (escape focus, latent subsidiary pacemaker activity)
top : Bradycardias
23 What is 1st degree Heart Block?
ECG Findings:
1. Prolonged PR interval
Dog PR > 0.13 sec
Cat PR > 0.09 sec.
2. P wave for every QRS and QRS for every P wave.
Etiology:
1. This disorder is due to prolonged conduction across the atrioventricular node.
2. Associated with disorders that cause increase parasympathetic tone.
3. May be normal.
4. PR increases with age and lengthens with rapid HR.
5. Drug therapy (digitalis, beta blocker, calcium channel blocker, procainamide, quinidine).
6. Hyperkalemia.
Consequences:
causes no hemodynamic abnormality
Treatment:
none required
Example of First Degree Heart Block in the Dog Place cursor on the image to see examples of the ECG
Findings
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10 fine lines vertically = 1 mv. (1cm = 1 mv); 50 fine lines horizontally = 1 sec. (50 mm/sec).
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Further Examples:
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1st Degree Heart Block example 1 (highlighted hints)
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top : Bradycardias
24 What is 2nd degree Heart Block?
Due to failure of the sinoatrial impulse after activating the atrial myocardium to activate the ventricular myocardium.
Depending on the location of the abnormality it may be classified as:
1. Mobitz type 1 (Wenckebach)
2. Mobitz type 2
Mobitz type 1 (Wenckebach):
1. ECG Findings:
1. P wave that is not followed by a QRS complex
2. QRS complex is usually of normal duration and morphology
3. The PR interval progressively prolongs just prior to blocked beat
4. When comparing the PR interval of the beat immediately preceeding the blocked beat with that of
the beat immediately following the blocked beat, the PR interval of the preceeding beat is longer
than the PR interval of the following beat.
Mobitz type 1: Place cursor on the image to see examples of the ECG Findings
This trace is of a dog; 10 fine lines vertically = 1 mv; 25 fine lines horizontally = 1 sec.
Further Examples:
Second Degree Heart Block: Mobitz Type 1 example 1 (highlighted hints)
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2. Etiology:
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1. Due to failure of the sinoatrial impulse to propagate through the atrioventricular node
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2. Excessive vagal tone can cause this abnormality
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4. Drug therapy (e.g. digitalis, beta blocker, calcium channel blocker)
3. Consequences:
1. Very rarely is the heart rate sufficiently reduced to cause any reduction in cardiac output.
2. This rhythm disturbance is important to distinguish from second degree heart block of the Mobitz
type II variety which is potentially much more severe.
4. Treatment:
1. None required
2. Atropine responsive
Mobitz Type 2: Place cursor on the image to see examples of the ECG Findings
1. ECG Findings:
1. P wave that is not followed by a QRS complex
2. May have a wide QRS complex (not shown in example)
3. PR interval of constant duration
4. May have multiple P waves that are not followed by QRS complexes (i.e. 2:1, 3:1, 4:1, etc. block)
Mobitz Type 2:
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(10 fine lines vertically = 1 mv; 25 fine lines horizontally = 1 sec.)
Further Examples:
Second Degree Heart Block Mobitz Type 2 example 1 (highlighted hints)
2. Etiology:
1. Due to failure of the sinoatrial impulse to propagate through the His bundle or bundle branches
2. Associated with organic disease of the His bundle or bundle branches. This may be in the form of an
ischemic area, scar, inflammation, infection with necrosis, neoplasia or granuloma
3. Consequences:
1. Evidence of reduced cardiac output may occur if the ventricular rate is substantially reduced:
dog with HR <40
cat with HR <60
4. Treatment:
1. Usually not responsive to atropine, Glycopyrrolate
2. The ventricular rate can usually be increased with intravenous isoproterenol
3. Unless the ventricular rate is slow, no treatment is required
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4. Permanent pacemaker implantation may be indicated in some cases
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1. Mobitz Type 2 2nd degree Heart Block is considered an important warning signal of the potential
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progression to 3rd degree Heart Block, which requires prompt attention.
2. Therefore it is important to distinguish between Mobitz Type 1 and Type 2 because Type 1 warrants little
concern but, Type 2 warrants continued monitoring to detect the onset of 3rd degree Heart Block
Dosages:
1. Atropine (parasympatholytic):
dog: 0.040.06 mg/kg (IV,IM); 0.04 mg/kg TID QID (SQ, PO)
cat: 0.020.04 mg/kg (IV,IM), QID (SQ)
2. Glycopyrrolate (parasympatholytic):
dog: 0.0050.01 mg/kg (IV,IM); 0.010.02 mg/kg BIDTID (SQ)
cat: 0.0050.01 mg/kg (IV,IM); 0.010.02 mg/kg (SQ)
3. Isoproterenol (betaagonist):
dog: 0.040.09 ug/kg/min (CRI)
cat: 0.040.09 ug/kg/min (CRI)
4. Terbutaline (betaagonist):
dog: 25 mg BID (PO)
cat: unknown
top : Bradycardias
25 What is 3rd degree Heart Block?
Example of Third Degree Heart Block in the Dog
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(10 fine lines vertically = 1 mv; 25 fine lines horizontally = 1 sec.)
ECG Findings:
1. The atrial rate and rhythm that occurs is independent of a much slower ventricular rhythm.
2. The atrial rate tends to be fast, and regular.
3. The ventricular rhythm is regular and much slower than the atrial rhythm.
dog ventricular rate approx. 40 60 bpm
cat ventricular rate approx. 90 110 bpm
4. The resultant ventricular activation is initiated from latent, subsidiary automatic pacemaker foci. The
resultant rhythm is referred to as an escape rhythm. If the escape ventricular activation occurs from a high
ventricular focus, the QRS morphology may look relatively normal. Usually, however, the QRS morphology
tends to be very abnormal.
Etiology:
1. Due to the same etiologies as for 2nd degree Heart Block Mobitz Type 2.
Consequences:
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1. Can cause all the signs of reduced cardiac output
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Treatment:
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1. Atropine is usually not effective.
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2. IV isoproterenol may increase the ventricular rate.
3. Pacemaker therapy is usually the only effective therapy.
4. Evaluation and treatment for hypothyroidism may be rewarding.
Dosage:
1. Isoproterenol:
2. Terbutaline:
dog: 25 mg BID (PO)
cat: unknown
top : Bradycardias
26 What is Sick Sinus Syndrome?
Sick Sinus Syndrome refers to a group of disorders involving the sinoatrial node usually with further involvement of
the atrioventricular node, His bundle and/or bundle branches. Frequently, multiple areas of the conduction system
are involved.
Paroxysms of sinus and supraventricular tachycardia may be interspersed among periods of bradycardia and
asystole.
Example of Sick Sinus Syndrome in the Dog
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ECG findings (may include any of the following):
1. A slow and irregular atrial rate (impaired sinoatrial activity), severe sinus bradycardia, or long pauses of
asystole with no escape beats.
2. Evidence of impaired atrioventricular conduction such that 2nd degree heart block is prevalent.
3. The ventricular rate is very slow and irregular.
Ventricular escape beats are common, though they are often slow to manifest (follow a longer pause
than usual).
4. Incomplete 3rd degree heart block may be present.
5. Paroxysms of supraventricular tachycardia alternating with severe sinus bradycardia.
Etiology:
1. May have SA nodal artery disease ischemia.
2. Fibrosis of SA node with partial involvement of the rest of conduction system.
3. Possibly inherited in some breeds as Miniature Schnauzer.
4. Usually idiopathic.
Consequences:
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1. periods of ventricular standstill are associated with syncope
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2. The paroxysms of supraventricular tachycardia may also cause syncope
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Treatment:
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1. Atropine is usually not effective.
2. IV isoproterenol may accelerate the ventricular rate.
3. Myocardial pacing (permanent pacemaker) is the only definitive therapy.
Dosages:
1. Atropine:
dog: 0.040.064 mg/kg (IV,IM); 0.020.04 mg/kg TIDQID (SQ,PO)
cat: 0.020.04 mg/kg (IV,IM), QID (SQ)
2. Isoproterenol:
Comments: Certain breeds are predisposed:
Miniature Schnauzers, especially females
Tachycardias
top : Tachycardias
27 What is sinus tachycardia?
Example of Sinus Tachycardia in the Dog
ECG Findings:
1. It is a sinus rhythm with an increased ventricular rate.
Dog (<20 kg) with heart rate >180 bpm
Dog (>20 kg) with heart rate >160 bpm
Puppies with heart rate >220 bpm
Cat with heart rate >240 bpm
Etiology:
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1. Pain
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2. Fever
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4. Reduced cardiac output (and resultant hypotension)
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5. Hyperthyroidism c u -tr a c k
6. Excitement
Consequences:
1. If HR is excessive, cardiac output may fall due to reduced diastolic filling time
2. Coronary perfusion decreases, also due to shorter diastole
3. Increased myocardial oxygen consumption per beat
If a normal heart is forced to beat at 250 bpm, it will experience myocardial failure in 34 weeks.
Treatment:
1. None required
2. Treat the underlying process
top : Tachycardias
28 What are supraventricular premature beats?
Example of Supraventricular Premature Beats in the Dog
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Further Examples:
Supraventricular Premature Beat example 1 (highlighted hints)
Supraventricular Premature Beat example 2 (highlighted hints)
ECG Findings:
1. Premature beats
2. The morphology of these beats usually looks very similar to the sinus beats
3. The duration of the QRS complexes are usually normal
Etiology:
1. These beats may originate within ectopic foci in the atria (socalled atrial premature beats) or they may
originate in the periAV nodal tissue (socalled junctional premature beats).
2. The causes of both types of supraventricular beats are identical:
due to disorders that result in enlargement of the atria
AV valve insufficiency
due to ischemic foci in the atria
drugs (digitalis, anesthetics)
Consequences:
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1. Several isolated premature beats are of no hemodynamic significance.
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2. However, when enough of these beats are present, a marked reduction in cardiac output may result.
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Treatment:
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1. Several isolated beats do not warrant therapy. However, such individuals should be frequently monitored for
exacerbation of their rhythm disturbance. In addition, attention should be directed toward identification and
management of the underlying disorder.
2. Criteria for therapy include:
1. if the animal is symptomatic with this disorder
2. if paroxysms of sustained tachycardia develop such as a burst lasting greater than 30 sec.
3. Drugs commonly used include
1. digoxin
2. beta blocker therapy:
propranolol
metoprolol
atenolol
3. calcium channel blocker therapy:
diltiazem
Dosages:
1. Digoxin:
dog: 0.22 mg/m2 BID (PO)
cat: 1/4 of 0.125 mg per cat (PO) q 2448h
2. Propranolol:
dog: 0.21.0 mg/kg TID (PO); 0.0240.06 mg/kg (IV) slowly
cat: 0.21.0 mg/kg BIDTID (PO); 0.04 mg/kg (IV) slowly
3. Metoprolol:
dog: 0.251 mg/kg BIDTID (PO)
cat: 0.251 mg BIDTID (PO) or 215 mg per cat TID (PO)
4. Atenolol:
dog: 0.251 mg/kg SIDBID (PO)
cat: 512.5 mg SIDBID (PO)
5. Diltiazem:
dog: 12 mg/kg TID (PO)
cat: 12 mg/kg TID (PO) or 7.5 mg per cat TID (PO)
Comment: Propranolol is a nonselective beta blocker with combined beta1 and beta2 blocking activity, whereas
metoprolol and atenolol are beta1 selective beta blockers at typical doses. Note that beta blockers and calcium
channel blockers are negative inotropes as well as negative chronotropes. Beta blockers in particular must be
started at low doses and uptitrated slowly.
Efforts to increase the parasympathetic tone and thereby reduce AV nodal conduction and slow the ventricular
response are useful to assist in detecting atrial activity (see P waves on ECG). This assists in the differentiation of
supraventricular ectopia and ventricular ectopia. This can be accomplished by:
1. Vagal maneuvers:
Ocular pressure.
Carotid sinus massage.
2. Parasympathomimetic agents:
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Edrophonium chloride.
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3. Reflex induced increase in vagal tone:
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29 What is supraventricular tachycardia?
Example:
ECG Findings:
1. A string of at least 4 supraventricular premature beats in a row.
2. Often occurs as paroxysms (bursts).
Etiology:
1. The same as for supraventricular premature beats (above).
Consequence:
1. Paroxysms of supraventricular tachycardia can result in syncope and heart failure .
Treatment:
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1. As for supraventricular premature beats (above).
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top : Tachycardias
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30 What is atrial fibrillation?
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General Remarks:
Atrial fibrillation is a supraventricular disorder associated with many microfoci of atrial myocardium acting as
ectopic foci or serving as small reentrant pathways and activating the adjacent atrial myocardium. Only the ectopic
foci that manage to depolarize close to the AV node successfully penetrate the AV node to activate the ventricles.
There is no coordinated atrial contraction in this disorder. The ventricular myocardium is activated at a very fast rate
and at irregular intervals.
ECG Findings:
1. Very rapid and irregular ventricular rhythm.
2. No distinct P waves; at times the baseline may show very fine baseline undulations which are called
fibrillation waves. Frequently these fibrillation waves are not apparent.
3. The QRS complexes are supraventricular in origin thus the QRS complexes tend to look of normal
morphology.
Example of Atrial Fibrillation in the Dog
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Another Example of Atrial Fibrillation in the Dog Place cursor on the image to see examples of the ECG
Findings
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It is important to note that an undulating baseline is not present in all cases of atrial fibrillation. It is equally important
to ensure that an undulating baseline is not confused with multiple unassociated P waves.
Further Examples:
Atrial Fibrillation example 1 (highlighted hints)
Atrial Fibrillation example 2 (highlighted hints)
Comments:
The hallmark ECG findings are the presence of an irregular rhythm and absence of P waves. As the heart rate
becomes very rapid, the rhythm approaches a regular rhythm; however, a slight irregularity remains present.
Although the heart rate is usually rapid, it can be slow if:
1. a giant breed of dog is involved
2. AV nodal disease coexists
3. digitalis, betablocker, or calcium channel blocker therapy is on board
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In that underlying ventricular myocardial disease is usually present, the morphology of the QRS is often wide and
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ST segment changes may be present.
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Etiology:
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1. Due to a very high number of microfoci or small reentrant pathways in the atria. They are competing to
activate the AV node.
2. Due to disorders associated with atrial dilation.
1. AV valvular insufficiency
2. Cardiomyopathy
3. Congenital heart disease
3. May occur in the absence of organic heart disease (usually giant breed dogs). These individuals usually
have slow to normal ventricular rates.
Consequence:
1. The rapid ventricular rhythm results in a fall in cardiac output due to excessive heart rate.
2. Cardiac output also falls due to a loss of atrial contraction. At rapid sinus rates, the atrial component to
ventricular filling can account for up to 30% of ventricular filling. At slower rates, the atria contribute relatively
little to ventricular filling.
3. The rapid heart rates also result in an increase in myocardial oxygen consumption. This can result in more
myocardial hypoxia which causes a reduction in inotropy and exacerbation of dysrhythmias.
Treatment:
Goals of therapy:
1. Convert the rhythm to a sinus rhythm.
although DC countershock cardioversion is possible, most individuals revert back to atrial fibrillation
because of the underlying atrial pathology
2. Slow the rhythm.
reduce the tachycardic effect on cardiac output
reduce the effect of loss of atrial filling by slowing the rate:
1. digitalis digoxin
2. beta blockers propranolol, metoprolol, atenolol
3. calcium channel blockers diltiazem is our typical drug of choice to slow the heart rate in
this disorder.
Comments:
Dogs with cardiomyopathy may be relatively asymptomatic until the development of atrial fibrillation
Dosages:
1. Digoxin:
dog: 0.22mg/m2 BID (PO)
cat: 1/4 of 0.125 mg per cat (PO) q 2448h
2. Propranolol:
dog: 0.21.0 mg/kg TID (PO); 0.0240.06 mg/kg (IV) slowly
cat: 0.21.0 mg/kg BID TID (PO); 0.04 mg/kg (IV) slowly
3. Metoprolol:
dog: 0.251 mg/kg BIDTID (PO)
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cat: 0.251 mg BIDTID (PO) or 215 mg per cat TID (PO)
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4. Atenolol:
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cat: 512.5 mg SIDBID (PO)
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5. Diltiazem: c u -tr a c k
dog: 1.02.0 mg/kg TID (PO)
cat: 1.02.0 mg/kg TID (PO) or 7.5 mg per cat (PO)
dog and cat IV: 0.10.2 mg/kg slow IV followed by 1.5 ug/kg/min CRI
6. Amiodarone:
dog: Initial dose: 1015mg/kg BID (PO) for 7 d; then 57.5mg/kg BID for 14d; then 7.5 mg/kg SID
cat: unknown
Comments:
Our first choice for treatment of atrial fibrillation is typically diltiazem (calciumchannel blocker). The target
heart rate for most canine patients is 140160 bpm, though this is very patient dependent (some patients
require higher heart rate than others to maintain adequate cardiac output). Note that both calciumchannel
blockers and beta blockers are negative inotropes as well as negative chronotropes. Beta blockers in
particular require starting at low doses and uptitrating very gradually.
A recent study of 18 dogs with advanced cardiac disease and atrial fibrillation showed that better rate
control was achieved with the combination of diltiazem and digoxin compared with either drug on its own
(Gelzer et al. JVIM 2009;23:499508).
Amiodarone is potentially one of the most efficacious antiarrhythmics in people, however it has a significant
adverse effect profile. In people, toxicity related to pulmonary pneumonitis is well documented in at least 6%
of cases. It appears that higher doses and longer duration of administration increase the likelihood of this
toxicity. In addition, hypo and hyperthyroidism, GI and hepatic toxicity are described. Our experience with
amiodarone in veterinary medicine is very limited. Reductions in heart rate and even conversion to sinus
rhythm have been reported in dogs receiving amiodarone. However, GI side effects, hepatotoxicity,
neutropenia, and thrombocytopenia have been described. CBC and chemistry must be monitored
frequently
top : Tachycardias
31 What are ventricular premature contractions?
VPCs are contractions due to an ectopic focus in the ventricular myocardium.
Example of Ventricular Premature Contractions in a Dog
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1. The QRS complexes are usually wide and bizarre.
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2. If several ectopic foci are present, the morphology of the QRS will vary with each focus (multiform VPCs).
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that follows VPCs.
4. A fusion beat is a QRS with a morphology that is neither identical to the sinus QRS, nor to a typical VPC. It
is also a QRS which occurs on time (i.e. it is not premature). It represents a fortuitous situation wherein part
of the ventricular mass was depolarized as a result of the sinus beat and the remainder of the ventricular
mass was depolarized as a result of the ectopic ventricular focus. Example of a fusion beat
5. An interpolated beat is a special form of VPC wherein the presence of the VPC did not interrupt the
underlying sinus rhythm.
6. As most VPCs are accompanied by a pause or delay prior to the onset of the next sinus beat, a time
measurement that includes the pause can be used to discriminate between VPCs and SVPCs. For a
representation please see diagram under question 34.
Etiology:
1. Associated with ventricular concentric hypertrophy or eccentric hypertrophy.
2. Associated with hypoxemic states as anemia, gastric dilation volvulus, heart failure.
3. Associated with metabolic derangements such as acidosis or hypokalemia.
4. Associated with trauma (traumatic myocarditis).
5. Associated with circulating cytokines in neoplastic and systemic inflammatory disorders.
6. Associated with drugs as digitalis, barbiturates, antiarrhythmic agents.
Consequence:
1. If enough premature beats are present, cardiac output may fall (dyssynergy of contraction).
2. May predispose to ventricular fibrillation.
Treatment:
1. Lidocaine:
dog: 24 mg/kg slow (IV), repeat 510 min. to maximum of 8 mg/kg; followed by 2575 ug/kg/min
(CRI)
cat: 0.251.0 mg/kg slow (IV) over 5 minutes
2. Oral lidocaine analogs:
Mexiletine:
dog: 48 mg/kg BIDTID (PO)
cat: undetermined
3. Procainamide:
dog: 68 mg/kg slow (IV) over 5 min; 2540 ug/kg/min (CRI); 820 mg/kg q 46 hr (IM), TID (PO) slow
release
cat: 820 mg/kg TID (PO)
4. Sotalol:
dog: 0.52 mg/kg BID (PO)
cat: unknown
5. Amiodarone:
dog: Initial dose:1015mg/kg BID (PO) for 7 d; then 57.5mg/kg BID for 14d; then 7.5 mg/kg SID
cat: unknown
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Comment: The intravenous drug of choice for treatment of ventricular tachycardia is typically lidocaine. Our first
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choice for oral therapy of VPCs is typically sotalol.
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Comment: Amiodarone is potentially one of the most efficacious antiarrhythmics in people, however it has a
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toxicity related to pulmonary pneumonitis is well documented in at least 6% of cases. It appears that higher doses
and longer duration of administration increase the likihood of this toxicity. In addition, hypo and hyperthyroidism are
described. GI and hepatic toxicity may occur. In dogs, GI side effects, hepatotoxicity, neutropenia, and
thrombocytopenia have been described. CBC and chemistry must be monitored frequently.
Comment: All antiarrhythmics have the potential to be proarrhythmic. This may particularly be the case with the
class 1 antiarrhythmics (sodium channel blockers).
top : Tachycardias
32 When should I begin therapy for premature ventricular contractions?
Therapy should be started if:
1. The patient is symptomatic due to the dysrhythmia (syncopal or weak or in heart failure due to the fast heart
rate)
2. You believe the patient's rhythm is in imminent danger of degenerating to ventricular fibrillation
3. You believe the patient is at risk of sudden death (either due to severity of the arrhythmia or the presence of
structural heart disease associated with sudden death)
Most of us have little difficulty determining if condition #1 is present. The most common problem is determining if
condition #2 or #3 is present. We used to believe that any of the following criteria suggested that a patient was at
risk of degenerating to ventricular fibrillation:
1. more than 20 VPCs per min.
2. presence of doublets or triplets
3. presence of multiformed VPCs
4. presence of runs of VPCs (more than 3 in sequence)
5. presence of socalled R on T phenomenon (very early premature beats)
Recent work suggests that these old criteria are likely not indicators of patients at risk of developing ventricular
fibrillation. Well why not institute antiarrhythmic therapy any way just to be safe? This "cover your ass"
approach would be useful if there were no deleterious effects to this type of medication.
Previous work in people with slightly weakened hearts and having ventricular premature beats and treated
with antiarrhythmic drugs potentially sheds light on this issue.
In 1989 and 1991 the results of the CAST Trial (Cardiac Arrhythmia Suppression Trial) were released. (N Engl J
Med 1989; 321: 40612 and 1991; 324: 7818)
Purpose: To compare the effect of Placebo vs Encainide vs Flecainide (both Class IC agents and the
best and safest agents available in people at the time to treat VPCs) on survival in patients with
ventricular arrhythmias and asymptomatic or minimally symptomatic LV dysfunction
Sample: 1498 people enrolled
857 assigned to receive encainide or its placebo, 641 assigned to receive flecainide or its placebo
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the encainide and flecainide patients vs placebo. Thus in asymptomatic or minimally symptomatic
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This important study demonstrated that oral antiarrhythmic therapy can actually exacerbate
arrhythmias and promote sudden death (the very disorder it was intended to prevent). It is likely that
drugs like the oral lidocaine analogs (mexiletine) and procainamide (Class 1 agents) may be
extremely proarrhythmic. The Class 3 antiarrhythmics sotalol and amiodarone are believed to be the
safest antiarrhythmics.
At present, only the beta blockers have been shown to reduce the risk of mortality in the setting of
unsustained ventricular tachycardia. It is likely that amiodarone and sotalol will also reduce the risk
of sudden death, however, survival studies are unavailable as yet in people.
Comment: It is our belief that heart rate may be the ultimate criteria predicting the malignancy of such dysrhythmias
(in individuals that are not hemodynamically embarrassed by this arrhythmia). If VPCs occur in the presence of an
excessive heart rate, this potentially represents a condition which has a high probability of progression to
ventricular fibrillation. However, if VPCs occur in the setting of a normal heart rate or a low heart rate, this situation
may not represent a threat of degenerating to ventricular fibrillation. The definitive importance of heart rate in the
presence of VPCs remains to be determined.
top : Tachycardias
33 What is ventricular tachycardia?
Example of Ventricular Tachycardia in the Dog
Ventricular tachycardia (VT) refers to runs of greater than 3 VPCs in sequence. VT may markedly reduce cardiac
output (through dyssynergy of contraction and high heart rate). Etiology is as for premature ventricular contractions
(see above). VT is treated as described under premature ventricular contractions. A number of cases of slow VT
(dogs with heart rates from 80 120 bpm) frequently have minimal hemodynamic consequences as a result of this
dysrhythmia and therefore warrant observation but not antiarrhythmic therapy.
top : Tachycardias
34 Outline criteria to assist in the differentiation of supraventricular and
ventricular premature beats.
In that supraventricular premature beats may conduct with aberrancy resulting in bizarre and wide morphologic
beats, the differentiation of supraventricular premature beats from ventricular premature beats can be very difficult.
Since therapy for one may be contraindicated in the other, it is important to attempt to differentiate these
abnormalities. Also the prognosis for one is different than that for the other. However "when all is said and done" at
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times we simply cannot separate these dysrhythmias.
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1. Morphology of QRS is usually similar to 1. Morphology of QRS is bizarre vs the
the sinus beats sinus beats
2. QRS is usually narrow 2. QRS is usually wide
3. SVPBs can't occur as fusion beats 3. VPBs may occur as fusion beats
So if the beat in question occurs as a fusion beat it must be a VPB
4. SVPBs can't occur as interpolated beats 4. VPBs may occur as interpolated beats
So if the beat in question occurs as an interpolated beat it must be a VPB
5. Atrial (P wave) and ventricular (QRS)
5. AV dissociation is usually present
activation are associated
Often the P waves cannot be visualized in the presence of tachycardia because they
are buried in the QRS or T waves.
6. Nonfully compensatory pause is present 6. Fully compensated pause is present
If the background rhythm is irregular (as with sinus arrhythmia or atrial fibrillation) we
can't use this criteria because we can't predict the duration of 2 normal R to R intervals
7. When supraventricular tachycardia occurs 7.When ventricular tachycardia occurs it
it tends to be very regular may be slightly irregular
8. A premature beat that follows a premature 8. A premature beat that follows a
P wave is always a SVPC premature P is never a VPC
The absence of a premature P does not discriminate between an SVPC and a VPC
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A refers to the time between two normal sinus beats close to the premature beat. B refers to the time between the
sinus beat just before the premature beat to the sinus beat just after the premature beat.
If A > B (this is called a noncompensatory pause), indicates the premature beat is a supraventricular beat.
If A < B (this is called a compensatory pause), indicates the premature beat is a ventricular beat.
Example of an Interpolated Beat (VPC)
Example of Premature Beats
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This is a lead II trace of a dog; 5 fine lines vertically = 1 mv; 25 fine lines horizontally = 2 sec.
Miscellaneous
top : Miscellaneous
35 What are the electrocardiographic signs of hyperkalemia?
General remarks:
Hyperkalemia results in:
1. Inhibition of atrial myocardial depolarization.
2. Slowing of heart rate.
3. Prolonging QRS duration; complexes may become bizarre.
4. Also known as atrial standstill.
5. Rhythm called sinoventricular rhythm.
6. The ECG is a poor substitute for serum potassium levels to determine the degree of abnormality.
ECG Findings:
1. From reduction of P wave amplitude and prolongation of PR interval to absence of P waves altogether.
2. Increase of QRS duration.
3. Increase of QT duration.
4. Slowing of heart rate.
5. T waves become tall and spiked.
6. Decreased R wave amplitude.
Example of Hyperkalemia in the Dog Place cursor on the image to see examples of the ECG Findings
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Etiology:
1. Addison's Disease.
2. Obstructive urinary disease.
3. Oliguric, anuric renal disease.
4. Acidosis.
5. Uncontrolled diabetic ketoacidosis.
Treatment:
1. Sodium bicarbonate.
2. Treat the underlying disease.
3. If using fluids, use NaCl.
4. Ca gluconate antagonizes the cardiotoxic effects of potassium.
Dosages:
1. NaHCO3:
dog: 12 mEq/kg (IV) slowly
cat: same
2. Ca gluconate:
dog: 0.5 mg/kg (IV) slowly
cat: same
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Prognosis:
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1. Excellent response to therapy.
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This disorder must be distinguished from "silent atrium". Silent atrium is a diffuse atrial myocardial disorder
wherein the atrial tissue is neither capable of initiating an impulse nor being activated. This disorder will not
respond to potassium reductive therapy.
The most specific ECG feature is the absence of P waves. At times these may be difficult to identify in the
frontal plane leads. The V leads are usually the best leads to illustrate P waves.
top : Miscellaneous
36 What are the electrocardiographic signs of myocardial hypoxemia/ischemia?
General Comments:
1. There are no specific ECG findings typical of hypoxemia.
2. Some vague findings may be noted and these may include:
wide QRS complexes
ST segment depression or elevation
tall T waves (<1/4 total QRS excursion)
notching of the R wave of the QRS complex (Microscopic Intramural Myocardial Infarctions or MIMI)
low amplitude QRS complexes
conduction disturbances with aberrant conduction leading to bizarre QRS complex morphology
Example of ST Segment Depression in the Dog
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Example of Microscopic Intramural Myocardial Infarctions (MIMI) in the Dog
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Further Examples of MIMIs:
Microscopic Intramural Myocardial Infarctions (MIMI) example 1 (highlighted hints)
Microscopic Intramural Myocardial Infarctions (MIMI) example 2 (highlighted hints)
top : Miscellaneous
37 What is the significance of low amplitude QRS complexes in the dog?
ECG Findings:
1. Total excursion of the QRS complex is reduced
<20 kg dog: <1 mv
>20 kg dog: <1.5 mv
2. Other rhythm disorders may be present
Example of Low Amplitude QRS in the Dog
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Further Examples:
Low amplitude QRS complexes example 1 (highlighted hints)
Low amplitude QRS complexes example 2 (highlighted hints)
Etiologies:
1. Pleural effusion
2. Pericardial effusion
3. Obesity
4. Hypothyroidism
5. Pneumothorax
6. Diffuse myocardial disease
7. Normal variation
Consequences:
There is no hemodynamic significance associated with low amplitude QRS complexes. The underlying
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problem may have significant hemodynamic impact.
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the underlying disorder should be sought out and treated
top : Miscellaneous
38 What is the significance of wide QRS complexes?
ECG Findings:
Dog: >0.06 seconds
Cat: >0.04 seconds
Rhythm is sinus
Example of Wide QRS Complexes in the Dog Place cursor on the image to see examples of the ECG Findings
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10 fine lines vertically = 1 mv; 50 fine lines horizontally = 1 sec. Note the presence of MIMI.
Etiologies:
1. Aberrant conduction (socalled Bundle Branch Block)
2. Myocardial hypoxemia/ischemia
3. Left ventricular enlargement
Consequences:
As per the underlying etiology. With aberrant conduction this may be an early sign to underlying myocardial
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disease or impending complete heart block.
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No specific treatment. Address the underlying etiology
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top : Miscellaneous
39 What is aberrancy?
Aberrancy refers to the abnormal coordination of activation of the two ventricles that occurs from an impulse
originating from a source above the bifurcation of the bundle branches (as opposed to impulses that arise below
the bifurcation of the bundle branches such as escape beats or VPCs). Aberrancy is often referred to as bundle
branch block. In the normal situation, the activation of the entire ventricular myocardium occurs in a coordinated
fashion such that the left ventricle and right ventricle are activated simultaneously. In the case of aberrancy, one of
the ventricles is activated before the other. Bundle branch block can be described as complete or incomplete.
What is complete bundle branch block?
This refers to that situation when the activation of one ventricle begins and is completed prior to activation of the
other ventricle.
Normal conduction through the heart
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During normal contraction of the heart, a wave of depolarization occurs in each ventricle simultaneously.
ECG characteristics
Supraventricular origin
Narrow QRS complexes
Normal MEA
Right bundle branch block
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During Right Bundle Branch Block there is a
lesion along the right bundle branch which prevents normal conduction down to the right ventricle. As a result, the
left ventricle depolarizes normally and then its wave of depolarization spreads to the right ventricle. Therefore, the
depolarization of the ventricles during bundle branch block takes longer to occur, resulting in wider QRS
complexes.
ECG characteristics
Wide QRS complexes
MEA points to RV
Left bundle branch block
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During Left Bundle Branch Block there is a lesion
along the left bundle branch which prevents normal conduction down to the left ventricle. As a result, the right
ventricle depolarizes normally and then its wave of depolarization spreads to the left ventricle. Therefore, the
depolarization of the ventricles during bundle branch block takes longer to occur, resulting in wider QRS
complexes.
ECG characteristics
Wide QRS complexes
MEA points to LV
How does aberrancy manifest electrocardiographically?
Aberrancy results in altering the morphology and duration of the QRS.
Morphology: can vary from a left ventricular originating VPC morphology to that of a right ventricular originating
VPC morphology.
Duration: the duration in dogs can vary from as short as 60 to 65 msec with incomplete bundle branch block to up
to 120 msec with complete bundle branch block.
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Right bundle branch block
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What are the causes of aberrancy?
Disorders of the bundle branches:
These may result in complete blockage of transmission down the bundle branch or merely a slowing of the speed
of transmission down one of the branches.
Physiological:
Any supraventricular premature beat that occurs that is markedly premature can result in aberrancy. Usually a
beat must be less than 300 msec after the preceding beat to result in aberrancy. The absolute degree of prematurity
required to induce aberrancy is variable and depends on prevailing autonomic nervous system tone and the cycle
length that precedes the premature beat. The longer the preceding cycle length, the less premature the premature
beat must be to induce aberrancy. The more premature the premature beat the greater the degree of aberrancy.
Supraventricular tachycardia:
Merely driving the heart rate fast in some individuals will induce aberrancy. This usually results in a slower
conduction in the right bundle branch compared with the left bundle branch.
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top : Miscellaneous
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40 Differentials for Abnormalities on the ECG
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If I find an abnormality on the ECG, what does it mean?
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The common approach to ECG texts dealing with interpretation is to provide a list of ECG disorders with a
description of the ECG findings for each. Therefore the practitioner is faced with attempting to match his/her test
ECG with one of the members of the long list of potential ECG disorders in the text. Although this is fine, I would like
to add a different approach which is based on the ECG abnormality as a starting point. In this approach which is
provided below, the practitioner notes any abnormalities present on the test ECG and is provided a differential list
of possible disorders for each. Hence a shortened list of potential disorders is provided.
1. What if there is no P wave?
Several situations must be differentiated if "absence of P waves" is the abnormality.
Is the P wave totally absent throughout the rhythm?
Is the P wave obscured or intermittently present?
Is the P wave absent for only one beat?
2. What if the P wave is totally absent throughout the rhythm?
Rule outs include:
a. Atrial fibrillation (note the QRS to QRS interval must be irregular; the heart rate is usually high
normal or elevated). Baseline undulations or f waves can be misinterpreted as P waves. If there is no
consistent P morphology (usually there are too many possible P morphologies to select from due to
the undulating baseline) and it/these are at variable distances before the QRS, then I suggest there
are no P waves.
b. Hyperkalemia (also called temporary atrial standstill) (note the QRS to QRS interval tends to be
regular; the heart rate tends to be low normal or slow)
c. Silent atrium (a disorder wherein the atrial myocardium is replaced by fibrous tissue, also called
permanent atrial standstill) (note the QRS to QRS interval tends to be regular; the heart rate tends to
be slow, the rhythm is called an escape rhythm)
d. Supraventricular tachycardia (in fact there is always a P wave associated with the QRS here but in
many cases the P wave is completely buried in the QRS or T wave such that we can't visualize it)
e. An idioventricular rhythm (looks like ventricular tachycardia but the rate is slow; looks like an
escape rhythm but is too fast). No P waves are present.
3. What if the P wave is obscured or intermittently present?
Rule outs include:
a. A very small P wave. The P wave can be difficult to see or find in some dogs and many cats
because it is very small. The chest leads tend to give the biggest P waves, so always check here
carefully.
b. A buried P wave. When the heart rate is fast the P wave can be buried in the preceding T wave.
Look for pauses in the rhythm (such as after a VPC) to check for P waves, or try to slow the heart rate
and look for P waves.
c. Ventricular tachycardia. Several P waves are usually observed intermittently in most cases; the
other P waves are buried in the QRS or T wave of the VPC.
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d. Sick sinus syndrome. Intermittent periods of pause with no P or QRS, or just no P waves with an
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4. What if the P wave is absent for only one beat?
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Rule outs include:
a. A premature ventricular contraction if the QRS occurs early (the QRS must meet the criteria for
VPC)
b. A supraventricular premature contraction if the QRS occurs early (the QRS must meet the criteria
for a supraventricular premature contraction)
c. A ventricular escape beat if the QRS occurs late (>1.2 sec) (the QRS must be wide and bizarre in
morphology) Example of a ventricular escape beat
d. A supraventricular escape beat if the QRS occurs late (>1.2 sec) (the QRS must be narrow and
similar to the sinus beats)
5. What if there is no QRS complex following the P wave?
Rule outs include:
a. 2nd degree heart block or 3rd degree heart block (P waves that are not followed by a QRS)
b. Sick sinus syndrome (often there are periods of absent P waves and QRS in addition to absent
QRSs following a P)
6. What if there is no T wave
Rule outs include:
a. Artifact. If a deflection looks like it might be a QRS, although perhaps somewhat bizarre, and there
is no T wave, then that deflection is not a QRS, it is an artifact. All depolarizations must have a
repolarization wave.
7. What if there is an unusual shaped P wave?
Several situations must be differentiated if the P wave is of an unusual shape:
Is there just one isolated P wave that is of an unusual shape?
Is the P wave of variable shapes and occurring in a pattern?
Is the P wave of a consistent unusual shape?
8. What if there is just one isolated P wave that is of an unusual shape?
Rule outs include:
a. A premature (ectopic) P wave (usually this occurs as an early P wave). This P wave may or may not
be followed by a QRS complex (the latter is an APC with block).
9. What if the P wave is of variable shapes and occurs in a pattern?
Rule outs include:
a. Wandering atrial pacemaker (there is usually a pattern, for example: the P wave might be tall (in
lead II) on the short cycles and absent, isoelectric or negative on the long cycles; usually occurs in
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the setting or sinus arrhythmia)
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10. What if the P wave is of a consistent unusual shape?
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a. An ectopic atrial rhythm (a normal P wave must be positive in lead II)
11. What if the QRS is of an unusual shape?
Several situations must be differentiated if the QRS is of an unusual shape:.
Is there just one isolated QRS that is of an unusual shape?
Is the QRS is of a consistent unusual shape?
12. What if there is just one isolated QRS that is of an unusual shape?
Rule outs include:
a. A fusion beat if there is a typical P wave with a normal or near normal PR interval (usually occurs in
the company of other examples elsewhere of VPCs)
b. A premature ventricular contraction if the QRS is early (the QRS must meet the criteria for VPC)
c. A supraventricular premature contraction if the QRS occurs early (the QRS must meet the criteria
for a supraventricular premature contraction) conducting with a slight (or more) degree of aberration.
d. A ventricular escape beat if the QRS occurs late (>1.2 sec) (the QRS must be wide and bizarre in
morphology) and it is not preceded by a P wave.
e. A supraventricular escape beat if the QRS occurs late (>1.2 sec) (the QRS must be meet the
criteria for a supraventricular beat) conducting with a slight (or more) degree of aberration.
f. A sinus beat that conducts with aberration (as bundle branch block). A normal P wave must be
present and associated with this QRS complex.
g. Artifact. Artifact may be present as any of the following: if it occurs between the end of the preceding
QRS and the first half of the T wave of that QRS (no real beat [normal or ectopic] can occur at this
time because the heart is refractory); if it fails to alter the underlying rhythm (however interpolated
VPCs can do this as well); or if it fails to be followed by a repolarization wave, this should usually be
a deflection in the opposite direction of the artifact wave (if a real T wave were to be present).
13. What if the QRS is of a consistent unusual shape? Rule outs include:
a. Bundle branch block if the rhythm is sinus or of supraventricular origin (the QRS meets the criteria
for right or left bundle branch block)
b. Ventricular tachycardia (the QRS meets the criteria for ventricular tachycardia)
c. Right ventricular enlargement (a supraventricular rhythm and the QRS is negative in lead two;
meets the criteria for right ventricular enlargement)
d. An escape rhythm. It could be supraventricular conducting with aberration or ventricular in origin.
e. An idioventricular rhythm. A form of slow ventricular tachycardia.
14. What if the QRS has a notch in it?
Rule outs include:
a. A MIMI is present (refers to microscopic intramural myocardial infarct) (the beats must be sinus in
origin or supraventricular origin)
b. Not significant if present on a VPC or a ventricular escape beat
XC e XC e
F- w F- w
c. Not significant if bundle branch block is present
PD
PD
er
er
!
!
W
W
O
O
N
N
y
y
15. What if the QRS is wide?
bu
bu
to
to
k
k
lic
lic
C
C
w
w
m
m
w w
w
w
Rule outs for a persistently wide QRS include:
o
o
.d o .c .d o .c
a. Left ventricular enlargement (if the R wave is tall then yes, left ventricular enlargement is present. If
the R wave is not tall then left ventricular enlargement may not be present). (with left ventricular
enlargement the QRS is only slightly widened)
b. A sick myocardium (dilated cardiomyopathy or heart failure can be associated with a wide QRS
associated with slow myocyte to myocyte conduction)
c. Bundle branch block (the rhythm meets the criteria for bundle branch block and the rhythm is sinus
or supraventricular) (the QRS is markedly widened)
d. Right ventricular enlargement (the QRS is only slightly widened or normal width)
e. Ventricular tachycardia (meets the criteria for VPC)
f. A ventricular escape rhythm
g. A preexcited beat (meets the criteria for preexcitation)
16. What if the QRS is small?
Rule outs include:
a. Thoracic effusions (pleural or pericardial)
b. A sick myocardium (dilated cardiomyopathy or heart failure can be associated with a low amplitude
QRS)
c. Obesity
d. Hypothyroid (probably related to obesity with hypothyroid)
e. Pneumothorax
f. A normal variant
g. A fusion beat; occurs as a single beat (meets the criteria for a fusion beat)
17. What if the R wave is tall in lead II?
Rule outs include:
Left ventricular enlargement (if the rhythm is supraventricular in origin)
18. What if the ST segment is depressed?
Rule outs include:
a. Left ventricular enlargement (if the left ventricular enlargement criteria are met; all by itself this is
probably not enough to suggest left ventricular enlargement)
b. A sick myocardium (dilated cardiomyopathy or heart failure can be associated with this)
c. Not of significance if not associated with a supraventricular beat (such as in a VPC)
d. Not of significance if associated with bundle branch block
19. What if the ST segment is elevated?
Rule outs include:
a. Pericardial disease
XC e XC e
F- w F- w
b. A sick myocardium (dilated cardiomyopathy or heart failure can be associated with this)
PD
PD
er
er
!
!
W
W
c. Not of significance if not associated with a supraventricular beat (such as in a VPC)
O
O
N
N
y
y
bu
bu
d. Not of significance if associated with bundle branch block
to
to
k
k
lic
lic
C
C
w
w
m
m
w w
w
w
o
o
.c .c
.d o
c u -tr a c k 20. What is there is coving of the ST segment? .d o
c u -tr a c k
Rule outs include:
a. A sick myocardium (dilated cardiomyopathy or heart failure can be associated with this)
b. This may be normal (many ECG units tend to produce some degree of coving)
21. What if the P wave is wide?
Rule outs include:
a. Left atrial enlargement
22. What if the P wave is tall?
Rule outs include:
a. Right atrial enlargement
b. Pulmonary artery hypertension
23. What if the P wave is notched?
Rule outs include:
a. Left atrial enlargement (only if the P wave is also too wide)
b. Normal variant (if the P wave is not too wide)
24. What if the P wave is not associated with the QRS?
Rule outs include:
a. 3rd degree heart block (the ventricular rate is slower than the atrial rate)
b. Ventricular tachycardia (the P waves are often difficult to observe as they are buried in the QRS or
T wave)
c. Non paroxysmal supraventricular (or junctional) tachycardia
d. Idioventricular rhythm
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QRS > 20 kg: < 0.06 < 0.04

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