Guide to Canine and Feline Electrocardiography E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1133

Veröffentlichungsjahr: 2018

Beschreibung

Guide to Canine and Feline Electrocardiography offers a comprehensive and readable guide to the diagnosis and treatment of abnormal heart rhythms in cats and dogs.  

• Covers all aspects of electrocardiography, from basics to advanced concepts of interest to specialists
• Explains how to obtain high-quality electrocardiograms
• Offers expert insight and guidance on the diagnosis and treatment of simple and complex arrhythmias alike
• Features numerous case examples, with electrocardiograms and Holter monitor recordings
• Shows the characteristics of normal and abnormal heart rhythms in dogs and cats
• Includes access to a website with self-assessment questions and the appendices and figures from the book

Leseprobe

Table of Contents

Cover

Preface

1 Anatomy of the Conduction System

Introduction

Sinoatrial node

The Atrioventricular Junction

Blood supply

Innervation

References

2 Cardiac electrophysiology

Introduction

Cardiac Cell Types

The Cardiac Action Potential

Resting Membrane Potential

Ion Channels, Exchangers and Pumps

Relevant aspects of Cardiac Cell Structure and function

Cell depolarisation and the Action Potential

Cell excitability and refractoriness

Pacemaker cells

Autonomic control of the Pacemaker Cells

Overdrive suppression of Pacemaker Cells

Atrioventricular Node Cells

Recommended reading

References

3 Cardiac vectors and the genesis of the electrocardiogram

Basic principles

Cardiac vectors

Electrocardiographic leads

Genesis of the electrocardiogram

References

4 Electrocardiography

Introduction

Procedure

ECG Machine Settings

Interpretation of the ECG

6. Mean Electrical Axis

Forming a Rhythm Diagnosis

Sample Form for ECG Report

References

5 Sinus rhythms

Introduction

Sinus rhythm

Cardiac structure and function

Sympathetic and Parasympathetic Influence on Sinus Node Depolarisation

Sinus rhythm

Sinus arrhythmia

Sinus bradycardia

Athletic heart

Sinus tachycardia

References

6 Pathogenesis and classification of arrhythmias

Introduction

Pathogenesis of arrhythmias

Abnormal Impulse Conduction

Anatomical substrates for arrhythmogenesis within the heart

Arrhythmia classification

Haemodynamic consequences of arrhythmias

Clinical signs that Commonly Accompany Cardiac Arrhythmias

References

7 Bradyarrhythmias and Conduction Disturbances

Introduction

Sinoatrial Node

Atrioventricular Block (AVB)

Intraventricular Conduction Disturbances

Sick Sinus Syndrome

Selected Conditions Resulting in Bradyarrhythmias

Other Causes of Bradyarrhythmia

Conclusion

References

8 Atrial Rhythms

Introduction

Atrial Ectopic Beats (AEBs)

Atrial Ectopic Beats, Ventricular Activation and the PR Interval

Ectopic Atrial Rhythms

Atrial tachycardia

Multifocal Atrial Tachycardia

Atrial Flutter

References

9 Atrial Fibrillation

Introduction

Mechanisms of Atrial Fibrillation

Factors Predisposing to Initiation and Maintenance of Atrial Fibrillation

Electrocardiographic Findings

Ambulatory ECGs in Atrial Fibrillation

Pathophysiology of Atrial Fibrillation

Situations When Atrial Fibrillation May Occur

Clinical Features of Atrial Fibrillation

Treatment

Targets for Ventricular Rate Control

Other Treatment Strategies

References

10 Junctional Rhythms

Introduction

Junctional Ectopic Beats

Junctional Rhythms

Atrioventricular Reciprocating Tachycardia

Macro Re‐entry Circuits in AVRT

References

11 Ventricular Rhythms

Introduction

Ventricular Ectopic Beats

Ventricular Rhythms

References

12 Clinical Approach to Arrhythmias and Intermittent Collapse

Introduction

Approach to Cases With a History of Intermittent Collapse

History in Cases With Intermittent Collapse

Comparison to Human Syncope

Fits, Faints and Falling Over

Differential Diagnosis of Syncope/Intermittent Weakness

Managing Owner Expectation

Clinical Examination in Cases With Intermittent Collapse

Diagnostic Testing in Cases With Intermittent Syncope

Resting and Ambulatory ECGs

Logical Approach to Evaluation of the ECG

Primary Versus Secondary Arrhythmias

Physical Manoeuvres

Case Examples

References

13 Diagnostic Approach to Narrow‐QRS Complex Tachycardia

Introduction

Stepwise Approach to the Differential Diagnosis of Narrow‐QRS Complex Tachycardias

References

14 Diagnostic Approach to Wide‐QRS Complex Tachycardia

Introduction

Stepwise Approach to the Differential Diagnosis of Wide‐QRS Complex Tachycardias

References

15 Ambulatory Electrocardiographic Recordings

Introduction

Common Indications for Obtaining an Ambulatory ECG

Types of Monitor for Obtaining an Ambulatory ECG

Analysis of Holter Recordings

Holter Findings in Normal Dogs

Changes in the Frequency of Ventricular Ectopy with Age

Normal Holter Findings in Cats

Diurnal Variation in Dogs and Cats

Ambulatory ECGs in the Assessment of Anti‐arrhythmic Treatment Efficacy

References

16 Heart Rate Variability

Introduction

Measurement of Heart Rate Variability

Linear Methods of Calculating HRV

Frequency Domain Analysis of Heart Rate Variability

HRV in Canine Heart Disease

HRV in Sick Sinus Syndrome

Heart Rate Variability in Cats

References

17 Anti‐arrhythmic Drugs

Introduction

Drug Classification

Class I

Class IA

Class IB

Class IC

Class II

Class III

Class IV

Other anti‐arrhythmic agents

Treatment of Bradyarrhythmias

References

18 Pacemaker Therapy

Introduction

Indications

Assessment of the Patient

Physics of Pacing

Pacemaker Terminology

Permanent Pacemaker Implantation

Dual‐chamber Pacing

Pacemaker Implantation

Complications

Outcome

Other Implantable Devices

References

19 Electrophysiology Studies and Catheter Ablation

Introduction

The Electrophysiology Laboratory

Overview of a Standard Electrophysiology Study

Recommended Reading

References

20 Arrhythmias in Canine Cardiomyopathies and Valvular Heart Disease

Introduction

Arrhythmias in Breed‐specific Cardiomyopathies

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

Treatment of Asymptomatic Boxers

Irish Wolfhound Cardiomyopathy

Dilated Cardiomyopathy in Great Danes and Newfoundlands

Arrhythmias Associated with Chronic Valvular Degenerative Disease (CVDD)

References

21 Arrhythmias in Feline Cardiomyopathies

Hypertrophic Cardiomyopathy

Ventricular Arrhythmias

Supraventricular Tachyarrhythmias

Bradyarrhythmias: Atrioventricular block

Bradyarrhythmias: Sinus Bradycardia

Other ECG Findings

Restrictive and Unclassified Cardiomyopathy

Arrhythmogenic Right Ventricular Cardiomyopathy

Dilated Cardiomyopathy

References

22 Inherited Ventricular Arrhythmias in German Shepherd Dogs

Introduction

Epidemiology

Clinical Presentation

Diagnosis

Mechanism of Arrhythmias

Treatment

Prognosis

References

23 Systemic Disease and Arrhythmias, Including Selected Non‐cardiogenic Causes of Collapse

Introduction

Autonomic

Myocardial Hypoxia

Electrolyte Abnormalities

Endocrinopathies

Abdominal and Systemic Disease States

Miscellaneous Systemic Disease States Associated with Arrhythmias

Arrhythmias in Association with Systemic Infectious Diseases

Trauma

Toxicity and Arrhythmias

Selected Non‐cardiac causes of Episodic Weakness and Collapse

Conclusion

References

24 Cardiac Arrhythmias and Anaesthesia

Introduction

Perioperative Cardiac Arrhythmias

Common Anaesthetic Drugs and Arrhythmias

Intra‐operative Arrhythmias: Specific Considerations in the Anaesthetised Patient

Summary

Key Points

References

Appendix 1: Normal Ecg Measurements for Cats and Dogs

Corrected QT interval (QTc)

References

Appendix 2: Arrhythmias – A Brief Review

General

P waves

QRS complexes

Sinus Rhythms

Ectopic Foci

Conduction Abnormalities

Tachycardias

Appendix 3: Mean Electrical Axis

Directions for Using Tables to Determine the Mean Electrical Axis

References

Appendix 4: Anti‐Arrhythmic Drugs and Dosages

Appendix 5: Sample ECG Reports

Self‐assessment

ECG Trace 1

ECG Trace 2

ECG Trace 3

ECG Trace 4

ECG Trace 5

ECG Trace 6

ECG Trace 7

ECG Trace 8

ECG Trace 9

ECG Trace 10

ECG Trace 11

ECG Trace 12

ECG Trace 13

ECG Trace 14

ECG Trace 15

ECG Trace 16

ECG Trace 17

ECG Trace 18

ECG Trace 19

ECG Trace 20

Index

End User License Agreement

List of Tables

Chapter 02

Table 2.1 Properties of membrane potentials in canine heart

Table 2.2 Ion currents and correspondent carriers involved in cardiac cell depolarisation and repolarisation

Chapter 04

Table 4.1 Standard limb positions and various electrode colour codes

Table 4.2 Time measurements according to paper speed

Table 4.3 Distance occupied by 3 and 6 s intervals at different paper speeds

Table 4.4 Normal reference ranges for cat and dog electrocardiographic measurements

Table 4.5 The normal QRS morphologies in different leads in order of frequency

Table 4.6 Formulae for correcting QT interval for heart rate

Table 4.7 Using the quadrant method to approximate the mean electrical axis

Table 4.8 Quick guide to making a rhythm diagnosis

Chapter 05

Table 5.1 Guide to heart rates for sinus rhythm, sinus bradycardia and sinus tachycardia in dogs and cats

Table 5.2 Sinus rhythm

Table 5.3 Sinus arrhythmia

Table 5.4 Sinus bradycardia

Table 5.5 Sinus tachycardia

Chapter 06

Table 6.1 Rhythm disturbances in dogs and cats

Chapter 07

Table 7.1 Anatomical classification of conduction disturbances in humans

49

Chapter 09

Table 9.1 Characteristics of atrial fibrillation

Chapter 10

Table 10.1 Focal junctional tachycardia

Table 10.2 Pre‐excitation

Chapter 11

Table 11.1 Characteristics of ventricular ectopic beats based on their origin

13

Table 11.2 Grading system proposed by Lown and Wolf to categorise the severity of ventricular arrhythmias

Chapter 12

Table 12.1 Potential causes of intermittent syncope in dogs and cats

Table 12.2 Tests frequently performed in the investigation of intermittent syncope with history and clinical findings suggesting a cardiac aetiology

Chapter 15

Table 15.1 Heart rates in normal dogs: minimum, maximum and mean heart rates reported in several studies using normal dogs of different breeds

Table 15.2 Normal ambulatory ECG findings in dogs

Table 15.3 Frequency of ventricular ectopy in normal dogs of different breeds

Table 15.4 24 h ambulatory ECG findings in normal cats

Chapter 16

Table 16.1 Time domain indexes

Table 16.2 Geometric measures of HRV

Table 16.3 Frequency domain indexes

Table 16.4 Time domain and frequency domain approximate correlates

Chapter 17

Table 17.1 Summary of Vaughan Williams anti‐arrhythmic drug classification

Table 17.2 Summary of the electrocardiogram (ECG) changes induced by class IA anti‐arrhythmic drugs

Table 17.3 Summary of the ECG changes induced by class IB anti‐arrhythmic drugs

Table 17.4 Summary of the ECG changes induced by class IC anti‐arrhythmic drugs

Table 17.5 Summary of the ECG changes induced by class II anti‐arrhythmic drugs

Table 17.6 Summary of the ECG changes induced by common class III anti‐arrhythmic drugs

Table 17.7 Summary of the ECG changes induced by diltiazem

Chapter 18

Table 18.1 Pacemaker system generic code adapted for veterinary medicine

Chapter 23

Table 23.1 ECG changes seen after administering potassium‐containing solution to healthy dogs

Table 23.2 ECG changes observed at different serum potassium concentrations in clinical cases

Table 23.3 Electrophysiological alterations, causes and ECG changes associated with electrolyte abnormalities

Table 23.4 Examples of plants and medications with anticholinergic properties

Chapter 24

Table 24.1 Common conditions in the perioperative environment that predispose patients to arrhythmias

6

Table 24.2 Summary of the predominant effects of α‐adrenoreceptor stimulation

Table 24.3 Interactions between anaesthetic agents and anti‐arrhythmic drugs (from human data)

31

Table 24.4 The most frequently reported arrhythmias in dogs and cats associated with the use of commonly used anaesthetic drugs, their underlying causes and a practical approach to managing them where necessary

Appendix 03

Table A3.1

Table A3.2

Table A3.3

Table A3.4

List of Illustrations

Chapter 01

Figure 1.1 Cardiac conduction system. The sinoatrial node, also known as the sinus node, is found in the wall of the right atrium at its junction with the cranial vena cava in the upper portion of the terminal groove (sulcus terminalis). It is connected to the atrioventricular node (AVN) located on the floor of the right atrium via the anterior (AIP), middle (MIP) and posterior (PIP) internodal pathways. Connections also exist between the right and left atria, of which Bachmann’s bundle and the inferior interatrial pathway (not illustrated) are the most important. Bachmann’s bundle runs in the upper portion of the atrial septum towards the left auricle. The inferior interatrial pathway is composed of fibres that are continuous with the right atrial myocardium at the level of the ostium of the coronary sinus (CSO) and with the left atrial myocardium from which they separate approximately 20–30 mm from the CSO. The AVN is continued by the Bundle of His that penetrates the fibrous skeleton of the heart and ramifies into the right (RBB) and left (LBB) bundle branches. The LBB is composed of anterior (AF) and posterior ramifications (not illustrated). The bundle branch subdivisions give rise to numerous small branches that spread all over the subendocardium of both ventricles, forming the Purkinje network that connects the conduction system to the working myocardium.

Figure 1.2 The atrioventricular junction. The atrioventricular junction may be divided into the proximal atrioventricular bundle (PAVB), the compact node and the distal atrioventricular bundle (DAVB). It is located on the floor of the right atrium in a triangular‐shaped area (triangle of Koch) formed caudally by the coronary sinus ostium (CSO) and with the tendon of Todaro and the tricuspid valve rim as its lateral boundaries. The posterior (PIP), middle (MIP) and anterior (AIP) internodal pathways join the atrioventricular junction via distinct atrionodal bundles forming the PAVB. The DAVB extends from the compact node approximately 3 mm to a branching point at the cranial edge of the tricuspid septal leaflet. Here, it penetrates the septum fibrosum of the cardiac fibrous skeleton bridging the atria and ventricles. The DAVB divides into the left (LBB) and right (RBB) bundle branches at the level of the upper portion of the interventricular septum beneath the non‐coronary and the right aortic leaflets. CVC, Caudal vena cava.

Figure 1.3 The divisions of the left bundle branch. The left bundle branch and its ramifications are illustrated in this picture with the left ventricle open as if cut across its free wall and looking into the septum. The left bundle branch runs in the subendocardium on the left side of the interventricular septum in close proximity to the aortic valve. The initial part (or trunk) is brush‐like in shape, approximately 4–7 mm in width and 2–6 mm in length. It ramifies into two main groups of peripheral branches: the

cranial group

, commonly referred to as the anterior fascicle, and the

caudal group

or posterior fascicle. The cranial group splits into a few small branches that run beneath the endocardium for approximately 10–15 mm until they change into bands that project into the ventricular cavity – pseudotendons. Once they reach the base of the cranial (anterior) papillary muscle, they spread to the cranial area of the left ventricle in a mesh pattern. The caudal group gives off a few small branches that run approximately 10–15 mm beneath the endocardium in parallel with each other like a chord until they change into pseudotendons projecting into the ventricular cavity towards the caudal (posterior) papillary muscle. From this point, the Purkinje fibres from the pseudotendons spread over the caudal area of the left ventricle.

Chapter 02

Figure 2.1 The intercalated disk. The intercalated disk is composed of specialised structures –

desmosomes

and

fascia adherens

– that form tight junctions creating a strong mechanical link between cells. The

gap junctions

provide a functional connection between cells that allows passage of ions.

Figure 2.2 Stages of the cardiac action potential and ionic currents. (A) Ventricular myocyte. (B) Pacemaker cell. Note that in ventricular myocytes, the action potential has five stages – 0, 1, 2, 3 and 4 – whereas in pacemaker cells stages 1 and 2 are absent.

Figure 2.3 The cardiac action potential of the various cardiac cells.

Figure 2.4 Cell refractoriness. RMP, Resting membrane potential; RRP, relative refractory period.

Figure 2.5 Pacemaker currents and action potential. During the resting state (stage 4), there is a spontaneous increase in membrane potential due to a combination of inward flow of Na

+

(I

f

, I

b

) and Ca

2+

(I

Ca

‐T

), and a reduction in outward flow of K

+

(I

k

). When the depolarisation threshold is reached at approximately −40 mV, L‐type Ca

2+

channels open, allowing Ca

2+

to enter the cell causing cell depolarisation (stage 0) until they become inactivated less than 1 ms later. Cell repolarisation then follows via outward flow of K

+

(I

k

).

Figure 2.6 Effect of sympathetic and parasympathetic stimulation on pacemaker cells. Sympathetic stimulation results in an increase in inward sodium (I

f

) and calcium (I

Ca

‐L

) currents via increased levels of cAMP inside the cell. The end result is a faster rate of depolarisation during stage 4, ultimately resulting in a faster heart rate. Additionally, under adrenergic stimulation there is a shift from the dominant P cells in the centre of the sinus node to the more peripheral T cells that have a lower diastolic resting membrane potential (they are more polarised), favouring maximal activation of the I

f

current. Parasympathetic stimulation causes an increase in outward K

+

currents during stage 4 via activation of acetylcholine–ligand potassium channels (I

KACh

). This reduction in intracellular K

+

leads to a lower resting membrane potential (hyperpolarisation), making it more difficult for the activation threshold to be reached and effectively lowering the heart rate.

Chapter 03

Figure 3.1 Appearance of the electrocardiographic deflections depending on the direction of the electrical current in relation to the exploring electrode (+). (A) If the electrical current moves towards the exploring electrode, a positive deflection is recorded. (B) If the exploring electrode is perpendicular to the direction of the electrical current, a positive deflection followed by a negative deflection is seen as the current moves towards the electrode initially and then away from it. (C) If the electrical current moves away from the exploring electrode, a negative deflection is recorded.

Figure 3.2 Illustration of the deflections recorded on the electrocardiogram during cell depolarisation. A cell is depicted with electrocardiographic electrodes on each extremity with the corresponding electrocardiographic trace below. (A) In the resting state, there is a prevalence of negative charges inside the cell in contrast to the outside compartment. Since there is no movement of electrical charges, the electrocardiograph records a flat line (baseline) without any positive or negative deflections. (B) As depolarisation starts, an area of the cell starts to fill up with positive charges (positive pole), whilst in the other end negative charges still prevail (negative pole). This creates an electrical dipole with a potential difference between both extremities of the cell. The electrocardiograph records this potential difference (voltage) as a deflection with its peak at maximal potential difference. (C) Once the entire cell is depolarised, there is no longer a potential difference between the cell extremities, and the electrocardiograph displays a return to baseline.

Figure 3.3 Depolarisation of neighbouring cells and respective individual depolarisation vectors (arrows).

Figure 3.4 Vector summation and subtraction and its effect on the electrocardiographic deflections. (A) Two vectors travelling in the same direction add up (1 + 2), resulting in a larger electrocardiographic deflection (3) than they would individually. (B) Two vectors of the same amplitude travelling in the exact opposite direction cancel each other out and do not cause a deflection on the electrocardiogram. (C) Two vectors travelling at an angle add or subtract energy.

Figure 3.5 The anatomical planes.

Figure 3.6 Bipolar leads forming Einthoven’s triangle. Electrodes are placed in the forelimbs and the left hindlimb to record leads I, II and III.

Figure 3.7 The unipolar leads. (See text for explanation.)

Figure 3.8 The hexaxial lead system. The combination of the bipolar and unipolar augmented leads forms the hexaxial system that allows the study of the electricity flow in the frontal plane. Taking the heart as the central point, the diagram illustrates the possible directions of electricity flow measured in angles. The location of the name of the lead corresponds to the position of the exploring electrode (+). This diagram is used to calculate the mean electrical axis of the heart that represents the average of the sum of all vectors during ventricular (or atrial) depolarisation (see chapter 4).

Figure 3.9 Lannek’s precordial lead system modified by Detweiler and Patterson. On the right side of the chest, an electrode is positioned at the 5

th

intercostal space at the level of the junction between the rib and the sternum (CV5RL). On the left side of the chest, an electrode is positioned at the 6

th

intercostal space at the level of the junction between the rib and the sternum (CV6LL), and another is positioned at the 6

th

intercostal space over the costochondral junction (CV6LU). A fourth electrode is positioned over the spinous process of the 7

th

thoracic vertebra (V10).

Figure 3.10 Wilson’s precordial lead system modified by Kraus

et al.

On the right side of the chest, an electrode is positioned at the 5

th

intercostal space at the level of the junction between the rib and the sternum (V1). On the left side of the chest, an electrode is positioned at the 6

th

intercostal space at the level of the junction between the rib and the sternum (V2); another is positioned at the level of the costochondral junction (V4), and another further up the same intercostal space at approximately the same distance between V2 and V4 (V6). Additional electrodes are then positioned approximately halfway between V2 and V4 (V3) and between V4 and V6 (V5).

Figure 3.11 Illustration of the electrocardiographic waves as seen in lead II of the electrocardiogram. The P wave represents atrial depolarisation. The Q, R and S waves together form the QRS complex that represents ventricular depolarisation. The J point represents the return to baseline after the QRS. The T wave is the result of ventricular repolarisation, and the U wave (normally not visible) is attributed to delayed repolarisation of the Purkinje or M cells of the myocardium. Between each wave, there is a return to baseline called a

segment

. The PR segment, from the end of the P wave to the beginning of the QRS, represents the time the impulse spends travelling through the AVN and His‐Purkinje. During the ST segment, from the end of the QRS to the beginning of the T wave, the myocardial cells are in stage 2 of the action potential, and actual contraction is occurring. The PR interval starts from the beginning of the P wave to the beginning of the QRS, and the QT interval from the beginning of the QRS until the end of the T wave.

Figure 3.12 Atrial depolarisation. The arrows represent the direction of the depolarisation wave which is recorded as a positive deflection in lead II of the electrocardiogram called the P wave.

Figure 3.13 Atrial depolarisation and the appearance of the P wave in all six leads. The P wave is positive in leads II, III and aVF (inferior leads) and negative in leads aVL and aVR. In lead I, it may appear as a positive, biphasic or isobiphasic wave.

Figure 3.14 T

a

wave. (A) Atrial repolarisation occurs at the same time as the QRS, and therefore the T

a

is not normally visible. (B) Holter recording showing non‐conducted P waves where the T

a

can be seen. [10‐year‐old, female neutered Greyhound dog with third‐degree atrioventricular block]

Figure 3.15 Ventricular depolarisation. (A) The left side of the septum is depolarised, creating a depolarisation wave upwards towards the right (arrows). This is recorded as negative deflection in lead II – the

Q wave

. (B) The free walls of both ventricles are depolarised next from the apex towards the base. The sum of the depolarisation vectors is recorded as a positive deflection in lead II – the

R wave

. (C) Finally, the base of the ventricles is activated with a depolarisation vector directed upwards. This may be recorded as a negative deflection in lead II – the

S wave

. (See text for more details.)

Figure 3.16 Representation of the main cardiac vectors resulting from the propagation of the wavefronts through the ventricles. Vector 1: The left side of the interventricular septum is depolarised first (≈5 ms) via divisions of the left bundle branches, and is followed by the right side of the septum (≈12 ms). This results in an initial depolarisation front travelling ‘upwards’ (caudal‐to‐cranial/ventral‐to‐dorsal) and towards the right. Vector 2: The impulse then reaches the apex of the ventricles (≈15–25 ms) and the base (≈40–45 ms) via the right and left bundles. The depolarisation wave travelling through the right ventricle has an ‘upwards’ (caudal‐to‐cranial/ventral‐to‐dorsal) direction and towards the right. Vector 3: Activation of the left ventricle occurs via the branches of the cranial (anterior) and caudal (posterior) fascicles. Synchronous activation of the left ventricular areas supplied by both fascicles results in a depolarisation vector travelling with a ‘downwards’ (cranial‐to‐caudal/dorsal‐to‐ventral) direction and towards the left. See text for a more detailed description. Please note that this illustration is very simplified and has the sole purpose of making it easier to understand these concepts.

Figure 3.17 Appearance of the QRS in all six leads. The appearance of the QRS in all six surface leads may be seen on the electrocardiographic trace on the right. On the left, the three ventricular depolarisation vectors discussed in Figures 3.15 and 3.16 are represented in the heart in the context of the hexaxial system to understand the appearance of the QRS waves on each lead. Depolarisation of the interventricular septum (vector 1 – red arrows) results in an initial depolarisation front travelling ‘upwards’ (caudal‐to‐cranial/ventral‐to‐dorsal) and towards the right. In leads I, II, III and aVF of the electrocardiogram (ECG), this appears as an initial negative deflection called the

Q wave

, although it is not always visible. In aVR it appears as a small positive wave (R instead of Q). In aVL it may not be visible or may appear as either a small negative or positive wave. It is followed by depolarisation of the right and left ventricles from apex to base. The depolarisation wave travelling through the right ventricle has an ‘upwards’ (caudal‐to‐cranial/ventral‐to‐dorsal) direction and towards the right (vector 2 in Figure 3.16), and synchronous activation of the left ventricle results in a depolarisation vector travelling with a ‘downwards’ (cranial‐to‐caudal/dorsal‐to‐ventral) direction and towards the left (vector 3 in Figure 3.16). Given that both ventricles are depolarised at the same time, the next wave recorded on the ECG corresponds to the sum of vectors 2 and 3, and since the mass of the left ventricle greatly exceeds that of the right ventricle, the resulting vector is directed ‘downwards’ (cranial‐to‐caudal/dorsal‐to‐ventral) and towards the left. In leads I, II, III and aVF, this results in a positive deflection – the R wave. In leads aVR and aVL, it appears as a negative deflection (S instead of R). The base of the ventricles is the last to be depolarised, resulting in a fourth vector directed ‘upwards’ (caudo‐dorsally; upward blue arrows at ventricle base). In humans, this may result in a small negative deflection on the ECG called the S wave. However, in quadruped animals, the direction of this vector is perpendicular to the frontal plane and is often not recorded on the hexaxial system.

Figure 3.18 Ventricular repolarisation. Epicardial cells achieve full repolarisation sooner than the endocardial cells, creating an electrical dipole that is registered on the electrocardiogram as the T wave.

Chapter 04

Figure 4.1 Patient positioning for electrocardiography (dog). (A) Adhesive electrodes can be attached to the digital pads or metacarpal/metatarsal pads. (B) If ‘crocodile’ clips are used, they can be placed on the skin over the olecranon in the forelimbs and over the patellar tendon in the hindlimbs. During a standard examination, the patient should always be in right lateral recumbency.

Figure 4.2 Examples of different types of ECG electrodes. Pre‐gelled self‐adhesive electrodes are more comfortable for the patient. If crocodile clips are used, their ends should be smoothed or slightly bent to avoid pinching the patient.

Figure 4.3 Patient positioning for electrocardiography (cat). With the cat in right lateral recumbency, adhesive electrodes are placed on the digital pads or metatarsal/metacarpal pads depending on their size.

Figure 4.4 Multiple ECG leads.

Figure 4.5 Different sensitivity settings, and effect on the ECG trace. [6‐year‐old, female neutered, Birman cat without evidence of heart disease] (50 mm/s)

Figure 4.6 Calibration spikes. At the start of a recording, many ECG machines will insert a calibration spike. The purpose of this spike is to show that the data conform to a standard format. The standard box varies between machines but is often 1 mV high and 200 ms wide (example at left: five small squares at 25 mm/s). If the R wave is very tall, then it may be necessary to halve the sensitivity, and this may be represented by the calibration spike containing a step on the left side (example in the middle). If the paper speed is set to 50 mm/s, the calibration spike will still be 200 ms wide (example at right: ten small squares at 50 mm/s).

Figure 4.7 Artefacts. (A) Muscle tremor. [10‐year‐old, female neutered, Schnauzer dog] (50 mm/s; 20 mm/mV) (B) Shivering artefact (red bracket). [10‐year‐old, female neutered, Schnauzer dog] (50 mm/s; 20 mm/mV) (C) Purring artefact. [10‐year‐old, male neutered, Tonkinese cat] (50 mm/s; 20 mm/mV)

Figure 4.8 Movement artefact. A sudden baseline shift is seen (arrow) due to limb movement. [11‐year‐old, male neutered, West Highland White Terrier dog] (50 mm/s; 10 mm/mV)

Figure 4.9 Breathing movement artefact. Oscillation of the baseline due to breathing movement. [9‐year‐old, male neutered, Ragdoll cat] (50 mm/s; 50 mm/mV)

Figure 4.10 Electrical interference. Regular, high‐frequency, sharp deflections of the baseline may be seen on electrocardiographic (A) and ambulatory ECG (Holter) (B) recordings due to electrical interference. The QRS complexes are visible in all leads, but P waves are not discernible on the electrocardiographic trace (A) and the first channel of the ambulatory ECG (Holter) trace. (A) [8‐year‐old, female neutered, Hungarian Vizsla dog] (50 mm/s; 20 mm/mV) (B) [2‐year‐old, male Lurcher dog]

Figure 4.11 Poor electrode contact. The baseline appears thicker with poor detail. [15‐year‐old, male neutered, Border Terrier dog] (50 mm/s; 20 mm/mV)

Figure 4.12 Normal electrocardiographic complex in lead II. The normal electrocardiographic complex is formed of a P, a QRS and T waves corresponding to atrial and ventricular depolarisations as well as ventricular repolarisation, respectively. The interval between the beginning of the P and QRS is the PR interval that corresponds to the time the impulse spends travelling through atria, the atrioventricular node and His–Purkinje before reaching the ventricular working myocardium. The QT interval represents the time necessary for ventricular depolarisation and repolarisation. The sections of return to baseline between the P and QRS and the QRS and T are the PR and ST segments.

Figure 4.13 Examples of different paper speeds. [2‐year‐old, female neutered, Border collie dog] (5 mm/mV)

Figure 4.14 How to calculate the instantaneous heart rate. The instantaneous heart rate may be calculated by determining the RR interval in milliseconds, and then dividing 60,000 by that number. This may be appropriate if the rhythm is regular, but with irregular rhythms the final result will be inaccurate in terms of how many beats actually happen in 1 min. [6‐year‐old, female, neutered Birman cat] (20 mm/mV)

Figure 4.15 How to calculate the heart rate with an ECG ruler. Many ECG rulers have two different scales, one for use at 25 mm/s and another for 50 mm/s. If that is the case, one cycle (one beat) should be counted from the arrow using the corresponding scale. In the example here, the scale on the ruler is for use with 50 mm/s but can still be used on a 25 mm/s trace by counting two cycles from the arrow instead of one. [6‐year‐old, female neutered, Birman cat] (20 mm/mV)

Figure 4.16 How to calculate the mean heart rate. To calculate the mean heart rate, one should count the number of beats in 3 s (75 mm at 25 mm/s and 150 mm at 50 mm/s) and multiply them by 20. Alternatively, count the number of beats in 6 s and multiply by 10 instead of 20. [6‐year‐old, female neutered, Birman cat] (20 mm/mV)

Figure 4.17 Where measurements are taken from a normal ECG complex. Measurements of the ECG complex are usually made from lead II, with the paper speed set at 50 mm/s and with the patient in right lateral recumbency. The amplitude is recorded in millivolts, and measurements of upward deflections are made from the upper edge of the baseline to the peak of the wave. For downward deflections, measurements are taken from the lower side of the baseline to the lowest point of the wave. The duration of a wave or segment of the complex is taken from start to finish. Measurements of duration are not influenced by patient position.

Figure 4.18 Variations in P wave morphology. (Positive) A P wave entirely above the baseline. (Negative) A P wave entirely below the baseline. (Bifid or notched) This describes a notch in the complex which does not cross the baseline. (Biphasic) This describes a P wave with unequal sections above and below the baseline, resulting in a wave that can be predominantly positive or negative; if equal components are seen above and below the baseline, the term

isobiphasic

may be used.

Figure 4.19 Changes in P wave amplitude and width suggestive of atrial enlargement. An increase in P wave amplitude (>0.4 mV in dogs and >0.2 mV in cats) is suggestive of right atrial enlargement, whereas an increase in P wave duration (>40 ms in dogs and in cats) suggests left atrial enlargement. If both are present, bi‐atrial enlargement may be suspected. It is important to note that, although these findings are suggestive of atrial enlargement, they are not always reliable and should not replace echocardiography for this purpose. If anything, they should prompt further investigation with echocardiography. [The examples here are from dogs.]

Figure 4.20 Examples of different QRS complex configurations and nomenclature. The first deflection of the QRS is termed Q, if it is negative and R if positive; a negative deflection after an R is termed S. A second positive deflection after an S is termed R’ (

R prime

). Additionally, if the amplitude of a deflection is less than 0.5 mV, a lowercase letter is used (q, r and s); if the amplitude is greater than 0.5 mV, capital letters are used (Q, R and S). This nomenclature is illustrated in the examples given here. Please note that this is not an extensive list and other conformations are possible.

Figure 4.21 Ventricular enlargement. (A) Electrocardiographic findings in a case with right ventricular enlargement (hypertrophy) due to severe pulmonary hypertension. The QRS complex shows deep S waves in leads II, III and aVF. The mean electrical axis (MEA) using either the quadrant or calculation method is −71° and therefore would be classified as a left axis deviation despite echocardiography demonstrating right‐sided enlargement. [7‐month‐old, male entire, German Shepherd dog] (50 mm/s; 10 mm/mV) (B) Electrocardiographic findings in a case with left ventricular enlargement (hypertrophy) secondary to severe subaortic stenosis. The QRS is wide (80 ms; >70 ms) with tall R waves in leads II (3.8 mV; >3.0 mV), III (3.4 mV) and aVF (3.4 mV; >3.0 mV); the MEA is normal (+90°). [7‐month‐old, male entire, German Shepherd dog] (50 mm/s; 5 mm/mV)

Figure 4.22 Mean electrical axis (MEA) in the horizontal (‘frontal’) plane in dogs. The normal MEA in dogs varies from +40° to +100°. Any dog with a MEA less than +40° is said to have a left axis deviation, whereas a right axis deviation is present if the MEA is greater than +100°.

Figure 4.23 Mean electrical axis (MEA) in the frontal plane in cats. The normal MEA in cats varies from 0° to +160°. A MEA less than 0° is said to be deviated to the left, whereas a right axis deviation is present if the MEA is greater than +160°.

Figure 4.24 The R wave amplitude in lead I is +0.8 mV, but the Q wave is −0.2 mV, so the net deflection is +0.6 mV. This is plotted on the positive arm of lead I, and a line drawn perpendicular to the measurement. This process is then repeated in lead III, where the R wave amplitude is +1.85 mV and the Q is −0.2 mV. This distance is plotted on the positive arm of lead III, and then a line is drawn perpendicular to this measurement and extended until it intersects the first line. The red line is projected from the centre outwards to the intersection of the perpendicular lines from leads I and III, and this gives the mean electrical axis.

Chapter 05

Figure 5.1 Twelve‐lead electrocardiogram during sinus rhythm in a dog. A normal (sinus) P wave is seen in all beats with an electrical axis of approximately 60°, consistent with an origin in the roof of the right atrium (+18° to +90°; positive wave in leads II, III and aVF; negative wave in leads aVL and aVR). The PR interval is consistent for all beats and within normal limits for a dog (≈100 ms; normal: 60–130 ms), suggesting normal atrioventricular conduction. A QRS is present after each P wave with a normal appearance (R wave in leads II, III and aVF; S wave in aVL and aVR) and duration (60 ms; normal: <70 ms), indicating normal intraventricular conduction and activation. [2‐year‐old, male neutered, Boxer] (50 mm/s, 5 mm/mV)

Figure 5.2 Sinus rhythm in a cat. Six‐lead electrocardiogram during sinus rhythm in a cat. A normal (sinus) P wave is seen in all beats with an electrical axis of approximately 65°, consistent with an origin in the roof of the right atrium (0 to +90°; positive wave in leads II, III and aVF; negative wave in leads aVL and aVR). The PR interval is consistent for all beats and within normal limits for a cat (≈70 ms; normal: 50–90 ms), suggesting normal atrioventricular conduction. A QRS is present after each P wave with a normal appearance (R wave in leads II, III and aVF; S wave in leads aVL and aVR) and duration (40 ms; normal: <40 ms), indicating normal intraventricular conduction and activation. [8‐year‐old, female neutered, Birman cat] (50 mm/s, 20 mm/mV)

Figure 5.3 Respiratory sinus arrhythmia. A sinus rhythm is seen characterised by P‐QRS‐T complexes of normal appearance and duration. A cyclical variation of the heart rate is seen with an acceleration and deceleration of the rate that were associated with inspiratory and expiratory movements, respectively. [5‐year‐old, male neutered, Staffordshire Bull Terrier dog] (25 mm/s, 10 mm/mV)

Figure 5.4 Ventriculophasic sinus arrhythmia. Holter recording showing a second‐degree atrioventricular block with 2:1 conduction. The interval between the P wave of the beat including the QRS and the blocked P (550 ms) is shorter than the interval between the blocked P and the following P (670 ms). This is suggestive of ventriculophasic sinus arrhythmia. The underlying mechanism is not fully understood; however, a positive chronotropic effect caused by the effects of atrial stretch during ventricular systole, and an increase in sinus node perfusion, are thought to elicit an earlier sinus depolarisation following ventricular contraction. A sensed increase in pressure by arterial baroreceptors following ventricular contraction is thought to elicit an increase in vagal tone, lowering the sinus node discharge rate in the subsequent beat. [11‐year‐old, male Labrador Retriever with second‐degree atrioventricular block]

Figure 5.5 Respiratory sinus arrhythmia with wandering pacemaker. A slightly irregular rhythm is seen due to respiratory sinus arrhythmia in this patient. The QRS appearance and duration are normal, suggesting a normal intraventricular conduction and activation. The P wave morphology is variable: during periods of higher heart rate (such as in the last three beats), it is normal, with origin in the roof of the right atrium (positive wave in leads II, III and aVF; negative wave in leads aVL and aVR); during periods of lower heart rate, the P wave amplitude is progressively reduced, with a shift in origin to areas lower in the right atrium (negative in leads III and aVR, whilst positive in aVL). The P wave duration (≈40 ms) and PR interval (≈120 ms) remain similar in all beats. This variation of the P wave morphology associated with the heart rate is described as

wandering pacemaker

. It is due to a shift in atrial activation via impulses originating in the dorsal areas of the sinus node during higher heart rates, and ventral areas of the sinus node during periods of lower heart rates. [9‐year‐old, female neutered, Boxer dog] (50 mm/s, 20 mm/mV)

Figure 5.6 Heart rate in an athletic dog. Tachogram recorded from an athletic dog showing that the mean heart rate was 57 bpm and therefore below the accepted range of 65–90 bpm. The resting heart rate was between 30 and 40 bpm. [6‐year‐old, male neutered, German short‐haired pointer]

Figure 5.7 P‐QRS‐T changes with tachycardia. Ambulatory ECG traces from the same dog during (A) sinus rhythm and (B) sinus tachycardia.

Figure 5.8 P and T wave superimposition during tachycardia. Ambulatory ECG trace from a dog during sinus tachycardia showing superimposition of the P and T waves as the heart rate increases. [6‐year‐old, female, neutered Greyhound dog]

Figure 5.9 Tachogram recorded from a young dog with suspicion of inappropriate sinus tachycardia. This dog was presented for suspicion of persistent tachycardia even during sleep. A 12‐lead electrocardiogram was consistent with sinus tachycardia, and a 24 h Holter monitor revealed tachycardia with P waves that had the same conformation during periods of higher and lower rates, also suggestive of a sinus rhythm. The minimum heart rate (95 bpm) and the average heart rate (125 bpm) were both above the expected range. [5‐month‐old, female Rhodesian Ridgeback dog]

Chapter 06

Figure 6.1 Mechanisms of enhanced normal automaticity. As the name suggests,

enhanced normal automaticity

refers to an increase in the discharge rate of pacemaker cells in the sinus node or subsidiary pacemakers above the expected range. The underlying mechanisms include an increase in the rate or slope of stage 4 depolarisation (top picture), a reduction in the activation threshold (middle picture) and a higher diastolic membrane potential (bottom picture). Enhanced normal automaticity can occur with excessive sympathetic stimulation or low potassium levels.

Figure 6.2 Mechanisms of abnormal automaticity. Occasionally, cardiac cells that are not normally capable of spontaneous depolarisation such as the working myocardium acquire the ability to depolarise spontaneously. This can occur with cell damage that impairs cell membrane function (especially the 3Na

+

/2K

+

ATPase pumps), causing an increase in the resting membrane potential (RMP) illustrated here. If the RMP increases to around −50 mV, inactivation of I

k

and activation of I

Ca‐L

currents may occur, leading to spontaneous cell depolarisation.

Figure 6.3 Representation of triggered activity. Triggered activity is characterised by premature depolarisation of the cell before it is fully repolarised. This occurs due to oscillations of the membrane potential during stages 2 or 3, or the beginning of stage 4, of the action potential. A premature depolarisation that occurs during stages 2 or 3 is termed an

early afterdepolarisation

(EAD), and during stage 4 is referred to as a

delayed afterdepolarisation

(DAD). EADs are caused by abnormalities that contribute to a higher than normal membrane potential during stages 2 and 3 of the action potential and also an increase in the action potential duration. DADs occur in circumstances where the cardiomyocyte cytoplasm is overloaded with Ca

2+

, such as intense sympathetic stimulation, ischaemia or digoxin toxicity. Intracellular hypercalcaemia stimulates oscillatory release of more Ca

2+

from the sarcoplasmic reticulum that subsequently favours a transient inward current of Na

+

, by either exchange with Ca

2+

(3Na

+

/1Ca

2+

exchanger) or activation of a non‐selective cation channel. This transient inward Na

+

current (I

TI

) results in premature depolarisation of the cell.

Figure 6.4 Anatomical re‐entry (see text for explanation).

Figure 6.5 Leading circle re‐entry.

Figure 6.6 Figure of eight re‐entry.

Figure 6.7 Reflection re‐entry.

Figure 6.8 Spiral wave re‐entry.

Chapter 07

Figure 7.1 Sinus pause. A sinus pause is seen during a period of bradycardia and respiratory sinus arrhythmia in a normal dog. The duration of this pause (1640 ms) is not a multiple of the preceding P‐P interval(s). [4‐year‐old, male neutered, Boxer dog without evidence of cardiovascular disease] (50 mm/s, 20 mm/mV)

Figure 7.2 Second‐degree sinoatrial block type II. A pause is seen with a duration of 1530 ms, which is three times the duration of the preceding P‐P interval (510 ms × 3). This suggests that during this pause, two additional sinus depolarisations occurred but were not able to exit the sinus node and trigger a beat. This is consistent with a second‐degree sinoatrial block type II. [9‐year‐old, male neutered, Boxer dog] (50 mm/s, 20 mm/mV)

Figure 7.3 Atrial silence (atrial standstill) or third‐degree sinoatrial block. A narrow‐QRS rhythm is seen with a rate of 100 bpm. P waves are not seen preceding the QRS complexes that have a normal appearance (QRS duration, 60 ms; MEA, 72°). Differential diagnoses would include atrial silence or standstill in which atrial depolarisation does not occur, accounting for the lack of visible P waves; third‐degree sinoatrial block, in which the sinus node depolarises but the impulse never reaches the atrial myocardium or remainder of the conduction system, and a junctional rhythm is responsible for ventricular depolarisation; a junctional rhythm with a rate higher than the sinus rate; and a sinoventricular rhythm that can be seen with hyperkalaemia in which atrial depolarisation does not occur, accounting for the lack of P waves, but sinus depolarisation and conduction through the normal conduction system still occur. In this case, atrial standstill associated with atrial myocarditis was suspected. [2‐year‐old, female neutered, Beagle dog with atrial myocarditis] (50 mm/s, 10 mm/mV)

Figure 7.4 Sinus arrest in a dog. Sinus tachycardia is seen on the left of the trace with a rate of approximately 150 bpm, and it is followed by a pause lasting over 2 s, terminated by a ventricular escape beat and then a junctional rhythm. This pause occurs abruptly during sinus tachycardia, lasts for more than three times the preceding P‐P interval and is interrupted by a subsidiary pacemaker, which is consistent with sinus node disease. [11‐year‐old, female neutered, Staffordshire Bull Terrier dog with sick sinus syndrome] (50 mm/s, 10 mm/mV)

Figure 7.5 Sinus arrest causing collapse. This trace was obtained from a Holter recording at the time of an episode of collapse in a dog with sick sinus syndrome. A period of sinus tachycardia (180–200 bpm) is seen, followed by a 6.88 s period of asystole. [8‐year‐old, male neutered, Jack Russell terrier dog with sick sinus syndrome]

Figure 7.6 Atrioventricular block in dogs. (Top) First‐degree atrioventricular block (1AVB) is characterised by a lengthening of the PR interval above >130 ms. (Middle two rows) Second‐degree atrioventricular block (2AVB) Mobitz type I is characterised by a progressive lengthening of the PR interval until an impulse is blocked in the atrioventricular node and the P is not followed by a QRS (arrow). This is also often referred to as a

Wenckebach‐type block

. In 2AVB Mobitz type II, one or more P waves are not followed by a QRS (arrow), but the PR interval of the conducted beats is constant. (Bottom) Third‐degree atrioventricular block (3AVB) is characterised by dissociation of the atrial and ventricular rhythms. All the atrial depolarisations are blocked in the atrioventricular node, and ventricular depolarisation occurs due to a junctional (50–60 bpm) or ventricular (30–40 bpm) escape rhythm. None of the P waves (arrows) are followed by a QRS, and this becomes apparent by the fact that the interval between the P and QRS is variable.

Figure 7.7 Atrioventricular block in cats. (Top) First‐degree atrioventricular block (1AVB) is characterised by a lengthening of the PR interval above 90 ms. (Middle) One or more P waves are not followed by a QRS (arrows), but the PR interval of the conducted beats is usually constant. (Bottom) Third‐degree atrioventricular block (3AVB) is characterised by dissociation of the atrial and ventricular rhythms, since all the atrial depolarisations are blocked in the atrioventricular node. A ventricular escape rhythm is often present with a rate between 110 and 140 bpm. None of the P waves (arrows) are followed by a QRS, and this becomes apparent by the fact that the interval between the P and QRS is variable.

Figure 7.8 Low and high‐grade atrioventricular block classification.

Figure 7.9 Right bundle branch block in a dog. A sinus rhythm is present with a rate of approximately 60 bpm. The QRS is wide (≈120 ms; >80ms) with large S waves in leads II, III, aVF; and R waves in leads aVR and aVL. A concomitant left anterior fascicular block may also be present given an R wave in lead I and a MEA ≈−80° (−60 to −90°). [10‐year‐old, male neutered, Cairn Terrier dog without echocardiographic evidence of structural heart disease] (50 mm/s, 5 mm/mV)

Figure 7.10 Right bundle branch block in a cat. A sinus rhythm is present with a rate of approximately 160 bpm. A normal P wave (20 ms; MEA, ≈70°) is present, preceding each QRS with a fixed PR interval within normal limits (80 ms). The QRS is wide (60 ms) with a right deviation of the MEA (≈−95°). [11‐month‐old, female neutered, Domestic Shorthair cat without evidence of structural heart disease] (50 mm/s, 20 mm/mV)

Figure 7.11 Example of Ashman’s phenomenon from an ambulatory ECG. Beats 1, 4 and 6 are conducted with a bundle branch block following a long R‐R interval (beats 2 to 3 and 4 to 5), followed by a short RR interval (beats 3 to 4 and 5 to 6) suggestive of Ashman’s phenomenon. All beats are sinus with a consistent PR interval. It is postulated that the right bundle branch has a longer refractory period than the left bundle branch, and therefore during the shorter cycle it has not had time to fully repolarise, hence the block.

55

Ashman’s phenomenon may also be observed at or near the onset of re‐entrant narrow‐QRS complex tachycardias due to the sudden shortening of the R‐R interval. [9‐year‐old, male Boxer dog]

Figure 7.12 Left bundle branch block in a dog. A sinus rhythm is present with a rate of approximately 80 bpm. A normal P wave (40 ms; MEA, 60°) is present, preceding each QRS with a fixed PR interval within normal limits (120 ms). The QRS is wide (≈120 ms; >80 ms) with a normal MEA (68°). The QRS is predominantly positive in leads I, II, III, aVF and V2 to V6. [8‐year‐old, male, Gordon Setter dog with preclinical dilated cardiomyopathy] (50 mm/s, 5 mm/mV)

Figure 7.13 Left anterior fascicle block (LAFB) in a cat. A sinus rhythm is present with a rate of approximately 150 bpm. A normal P wave (30 ms; MEA, 82°) is present, preceding each QRS with a fixed PR interval within normal limits (60 ms). The QRS duration is slightly longer than normal (≈45–50 ms; <40 ms), with a left MEA deviation (−80°; −45 to −90°). Deep S waves (rS complexes) may be seen in leads II, III, and aVF, with qr and qR complexes in leads I and aVL, respectively. [16‐year‐old, male neutered, Bengal cat with equivocal hypertrophic cardiomyopathy] (50 mm/s, 50 mm/mV)

Figure 7.14 Intermittent bundle branch block in a dog. This ambulatory ECG trace shows a sinus rhythm with varying QRS complex morphologies. The coupling between the P waves and QRS complexes is consistent in all beats, suggesting sinus rhythm (or sinus arrhythmia) with an intermittent intraventricular conduction disturbance resulting in the wide‐QRS complexes (complexes 3, 4 and 5). The bundle branch block occurs when the heart rate increases, suggesting a phase 3 or acceleration‐dependent block. [9‐year‐old, male neutered, Boxer dog]

Figure 7.15 Supernormal conduction. This ambulatory ECG tracing was recorded from a dog with persistent left bundle branch block. A sinus rhythm is seen with a wide QRS (≈80 ms) in all beats except for the seventh beat, which presents a shorter duration (≈60 ms) which was unexpected. This beat was premature and is likely to have occurred during the supernormal excitability period, accounting for its normal or less aberrant conformation. [6‐year‐old, male, crossbreed dog]

Figure 7.16 Sick sinus syndrome. Example of an ambulatory ECG recorded from a dog with sick sinus syndrome. Periods of sinus rhythm and short paroxysms of narrow‐QRS tachycardia are abruptly interrupted by frequent long pauses. [12‐year‐old, female neutered, West Highland White Terrier with SSS]

Figure 7.17 Sinus node dysfunction in a cat with bradycardia detected as an incidental finding. Ambulatory ECG recording from a cat showing two sinus beats followed by a ventricular escape rhythm with a rate of 100 bpm. P waves are seen intermittently and highlighted by arrows. [4‐year‐old, neutered, male Domestic Shorthair cat]

Figure 7.18 Neurally mediated syncope. Example of ambulatory ECG during an episode of syncope in a Boxer. Prior to the event, the trace shows sinus rhythm with a rate of approximately 140 bpm, and this is followed by an abrupt transition to sinus bradycardia with a minimum instantaneous rate of 14 bpm, followed by a gradual return to sinus rhythm.

Chapter 08

Figure 8.1 Different P’ wave morphologies depending on the ectopic site location.

Figure 8.2 Atrial premature complex (*) followed by a compensatory pause. (50 mm/s; 5 mm/mV)

Figure 8.3 Atrial premature complex (*) followed by a non‐compensatory pause. (50 mm/s; 5 mm/mV)

Figure 8.4 Interpolated atrial premature complex (*). (50 mm/s; 5 mm/mV)In Figure 8.4, the underlying rhythm was sinus with a variable cycle length (P‐P) due to respiratory sinus arrhythmia. The third beat was an ectopic atrial beat but was not followed by a pause, which implies that it did not interfere with either the AVN and or sinus node activities. This was an interpolated beat.

Figure 8.5 Atrial bigeminy. The * highlights the premature beats which alternate with the sinus beats. [6‐year‐old, female neutered, crossbreed dog without obvious structural heart disease] (50 mm/s; 10 mm/mV)

Figure 8.6 Atrial couplet – two consecutive atrial ectopic beats (*). [10‐year‐old, male Giant Schnauzer with lymphoma and no obvious structural heart disease]

Figure 8.7 Atrial triplet – three consecutive atrial ectopic beats (*). [10‐year‐old, male Giant Schnauzer with lymphoma and no obvious structural heart disease] (50 mm/s; 10 mm/mV)

Figure 8.8 Blocked atrial premature contraction. (A) Ectopic atrial beat (*) with a prolonged P’Q attributed to slower conduction through the atrioventricular node. (B) Example of an ectopic atrial beat from the same patient without prolonged P’R. [6‐year‐old, female neutered, crossbreed dog without obvious structural heart disease] (50 mm/s; 10 mm/mV)

Figure 8.9 Example of a ‘hidden’ P’ wave (6‐lead trace available online). The fourth, sixth and tenth beats are ectopic, originating from the roof of the right atrium. The P’ wave of the sixth and tenth beats is superimposed on the T wave, resulting in an increase in amplitude in comparison to the T wave conformation of the normal beats. [6‐year‐old, female neutered, crossbreed dog without obvious structural heart disease] (50 mm/s; 10 mm/mV)

Figure 8.10 Ectopic atrial rhythm. The first five beats are sinus in origin (P axis of +64°) with a heart rate of approximately 100 bpm and a regular rhythm. From beat 6 to beat 10, there is an ectopic atrial rhythm originating from the roof of the left atrium (P’ axis of +127°) with a heart rate of approximately 120 bpm and a regular rhythm. The change in P wave morphology is most obvious in leads I and aVL (arrows). [8‐year‐old, female neutered, Great Dane with dilated cardiomyopathy] (50 mm/s; 10 mm/mV)

Figure 8.11 Atrial parasystole. A concomitant ectopic atrial rhythm (P’ and red dot on laddergram) and sinus rhythm (P and black dot on laddergram) can be seen. As illustrated on the laddergram, the cycle length of the ectopic rhythm (P’‐P’) is approximately 460 ms; when it is interrupted by a sinus beat (beat 6), the following ectopic beat occurs at an interval of 930 ms which is approximately double 460 ms. This suggests that the sinus depolarisation did not reset the ectopic focus (entrance block) and that it continued to discharge at the same rate. This is a feature of atrial parasystole in which the P’‐P’ interval is a multiple of a common denominator that is the discharge rate of the ectopic focus. [11‐year‐old, male Gordon Setter with suspicion of inflammatory myocardial disease] (50 mm/s; 10 mm/mV)

Figure 8.12 Atrial dissociation. (A) Electrocardiographic trace showing a narrow‐QRS tachycardia with an irregular rhythm and a ventricular rate of approximately 140–160 bpm. Waves consistent with P waves may be seen (P) and appear dissociated from the QRS complexes. The atrial depolarisation rate is approximately 200 bpm. Additional small undulations of the baseline may be seen. (B) Echocardiographic pulsed‐wave Doppler image showing the mitral inflow pattern in the same patient. Passive early diastolic flow (E waves) from the left atrium to the left ventricle may be seen, but flow resulting from atrial contraction (A waves) is not present in contrast to the tricuspid flow pattern from the same patient shown in (C), where both early diastolic filling (E waves) and flow resulting from organised atrial contraction (A waves) may be seen. These findings suggest the presence of a disorganized atrial rhythm (atrial fibrillation) at the level of the left atrium, whilst an organized rhythm (sinus or ectopic rhythm) is present on the right atrium as a result of atrial dissociation. [7‐year‐old, male neutered, Newfoundland dog referred for investigation of cardiac arrhythmia without evidence of structural heart disease]

Figure 8.13 Focal atrial tachycardia (FAT). Beats 4 and 5 are sinus beats, whilst the remainder are ectopic atrial beats originating from the floor of the right atrium (P’ axis of +30° and PR of 100–120 ms). From the sixth beat, an episode of FAT starts with a rate of 220 bpm. From beats 8 to 14, the P wave appears superimposed on the T wave. [10‐year‐old, male Border Terrier without obvious structural heart disease]. (50 mm/s; 10 mm/mV)

Figure 8.14 Multifocal atrial tachycardia. (A,B) Extracts of two distinct narrow‐QRS tachycardia episodes identified in the same patient. The P’ wave (arrows) conformations are different, as is the cycle length of tachycardia: 220–240 ms in (A) and 200–220 ms in (B). (C) An extract of sinus rhythm of the same patient for comparison. An electrophysiology study confirmed the presence of three distinct ectopic foci along the terminal crest. [6‐year‐old, male Hamilton Hound without obvious structural heart disease] (50 mm/s; 20 mm/mV)

Figure 8.15 Cavotricuspid isthmus–dependent atrial flutter. The depolarisation wave travels in a loop around the atrial septum, the lateral wall of the right atrium and the tricuspid annulus. It traverses an area of slower conduction between the ostium of the caudal vena cava, the Eustachian ridge and the tricuspid annulus termed the

cavotricuspid isthmus

(CTI). Most commonly, the direction of travel is counterclockwise –

typical flutter

– although it may also occur in a clockwise fashion –

reverse typical flutter

. RA, Right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle; Cd VC, caudal vena cava; Cr VC, cranial vena cava; CTI, cavotricuspid isthmus.

Figure 8.16 Typical atrial flutter. Flutter waves (F) can be seen in a characteristic sawtooth pattern. After each QRS, an F wave is superimposed with a T wave (T), causing small variations in its appearance. [9‐year‐old, female Bernese Mountain dog without obvious structural heart disease] (50 mm/s; 20 mm/mV)

Figure 8.17 Reverse typical atrial flutter. Flutter waves (F) can be seen with the appearance of a sine wave and a return to baseline. After each QRS, an F wave occurs superimposed with a T wave (T) appearing as a small positive deflection in lead II, although in some areas the real appearance of the T wave is disclosed by separation of the two waves. [10‐year‐old, male neutered, Bull Terrier with mitral valve dysplasia] (50 mm/s; 10 mm/mV)

Figure 8.18 Atrial fibrillo‐flutter or fibrillatory conduction. A narrow‐QRS tachycardia can be seen with an irregular rhythm and a rate of approximately 200 bpm. P waves are not discernible, and instead undulations of the baseline can be seen suggestive of atrial depolarisation waves; in leads III and aVL, these waves seem relatively organised and have an appearance suggestive of flutter waves, but closer analyses reveal that their cycle length is not constant and that this is indeed atrial fibrillation. [13‐year‐old, male neutered, Cocker Spaniel with chronic valvular degenerative disease] (50 mm/s; 10 mm/mV)

Figure 8.19 (A) Atrial flutter with 1:1 conduction. Narrow‐QRS complex tachycardia with a heart rate of 425 bpm. (B) After treatment with intravenous verapamil, flutter waves (F) are now visible with a change in atrioventricular conduction ratio to 3:1 and 4:1, resulting in a heart rate of 120–130 bpm. The flutter rate (F‐F interval) remains at 425 bpm [12‐year‐old, male neutered, Irish Setter without obvious structural heart disease]. (50 mm/s; 5 mm/mV)

Chapter 09

Figure 9.1 Multiple wavelet model. Multiple wavelets of electrical activity propagate within the atria due to functional re‐entry circuits (red arrows). A minimum number of wavelets (usually six or more) must coexist for AF to be maintained. These wavelets travel in different directions, depolarising small areas of atrial tissue, colliding with each other and then dividing or extinguishing one another in a random fashion.

Figure 9.2 Focal activation model. One or multiple ectopic atrial foci or micro re‐entry circuits are present (dark blue stars), and they discharge so rapidly that conduction through the atria cannot occur uniformly and the wavefronts break into irregular wavelets (red arrows).

Figure 9.3 The atrioventricular node and atrial fibrillation. Diagram illustrating four concomitant depolarisation waves (coloured arrows) reaching the atrioventricular node (AVN) at the same time. Each of these waves causes depolarisation of an area of the AVN tissue depending on their point of entry (coloured areas). The yellow, green and purple waves are cancelled out as they reach areas of refractory tissue. The red wave is able to traverse the AVN and goes on to depolarise the ventricles via the His–Purkinje system. The AVN acts as a filter, allowing only a few of the depolarisation waves to actually reach the ventricles and preventing the ventricular rate from being so high that it would be incompatible with life. The depolarisation waves that reach the ventricles do so in a random way that accounts for the irregularity of the ventricular response seen in atrial fibrillation. LBB, Left bundle branch; RBB, right bundle branch.

Figure 9.4 Atrial fibrillation. Narrow‐QRS complex tachycardia with irregular R‐R intervals, no discernible P waves and visible f waves (f) typical of atrial fibrillation. [7‐year‐old, male German Shepherd dog] (Lead II, 50 mm/s, 10 mm/mV)

Figure 9.5 Coarse atrial fibrillation. The f waves have higher amplitude with more of a sine wave appearance. [18‐year‐old, male neutered, crossbreed dog with chronic valvular degenerative disease] (Lead II, 50 mm/s, 50 mm/mV)

Figure 9.6 Fine atrial fibrillation. The f waves are not readily visible, although the irregularity of the rhythm and absence of visible P waves signal the presence of atrial fibrillation. [11‐year‐old, male neutered, Norfolk Terrier dog with chronic valvular degenerative disease] (Lead II, 50 mm/s, 10 mm/mV)

Figure 9.7 Wide QRS in atrial fibrillation secondary to ventricular enlargement or hypertrophy. Atrial fibrillation in a dog with dilated cardiomyopathy. The QRS complexes are wide (75 ms) due to left ventricular enlargement. [9‐year‐old, male neutered, Saint Bernard dog with dilated cardiomyopathy] (Lead II, 50 mm/s, 5 mm/mV)

Figure 9.8 Wide QRS in atrial fibrillation attributed to a left bundle branch block. In this case, the QRS complexes were wide (80–85 ms), with an absence of precordial concordance suggesting a left bundle branch block. Concordance exists when all the QRS complexes in the chest leads are either predominantly positive or predominantly negative (see chapters 7 and 14). The QRS duration was thought to be excessive due to left ventricular enlargement. [7‐year‐old, female crossbreed dog with a patent ductus arteriosus] (50 mm/s, 5 mm/mV)

Figure 9.9 Atrial fibrillation accompanied by ventricular ectopic beats. Ventricular ectopic beats (*) occur randomly and do not follow the long RR–short RR sequence observed in Ashman’s phenomenon. A post‐extrasystolic pause may also be observed due to occult retro‐conduction of the ventricular impulse through the atrioventricular node as shown in the example above (fourth beat from left). A tendency to organization into couplets, triplets, bigeminy, trigeminy and runs of tachycardia is also observed with ventricular arrhythmias.

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[8‐year‐old, male Golden Retriever dog] (50 mm/s; 10 mm/mV)

Figure 9.10 Atrial fibrillation with pre‐excitation. The QRS complexes are wide (85–90 ms) except for the 15th beat (*), which presents a normal duration (60 ms). A positive deflection may be seen in the initial portion of the R wave consistent with a delta wave (δ, highlighted by arrow), particularly in lead III (arrows). The RR intervals are irregular, as would be expected in AF and allowing differentiation with ventricular tachycardia.

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This dog also presented periods of atrial fibrillation without pre‐excitation. [9‐year‐old, male neutered, Boxer dog] (50 mm/s; 5 mm/mV)

Figure 9.11 Atrial fibrillation and complete atrioventricular block. The baseline shows fine undulations typical of f waves. The QRS complexes exhibit variable width and morphology, likely reflecting change in the site of the ventricular escape focus. Despite the presence of atrial fibrillation, the ventricular rhythm is regular as none of the impulses are conducted from the atria to the ventricles. [7‐year‐old, male Labrador Retriever dog] (Leads I‐III; 25 mm/s; 10 mm/mV)

Figure 9.12 Tachogram from a dog with rapid atrial fibrillation after treatment of congestive heart failure. The average ventricular rate over 24 h is 156 bpm, suggesting that this patient could benefit from anti‐arrhythmic treatment to lower the ventricular rate. Frequent peaks of elevated heart rate are also seen – for example, around 16:00. [7‐year‐old, male neutered, Labrador Retriever dog]

Figure 9.13 Tachogram from dog with lone atrial fibrillation The average 24 h ventricular rate is 87 bpm (blue circle). The right‐hand

y

‐axis shows the frequency of ventricular ectopy plotted against time on the

x

‐axis. Over the 24 h recording, there was minimal ventricular ectopy that occurred singly as escape beats during periods of low heart rate, and these beats occurred most frequently between 04:00 and 05:00 (red arrow). [5‐year‐old, male German Shepherd dog]