3D Cardiology in small animals: Pathophysiological basis and diagnostic keys

Medicina pediátrica en pequeños animales

Presentation brochure

3D Cardiology in small animals Pathophysiological and diagnostic key concepts

Pablo Gómez ochoa Iván SoSa SamPer

3D images anD augmenteD reality

3D Cardiology in small animals:

3D Cardiology in small animals Pathophysiological and diagnostic key concepts

Pathophysiological basis and diagnostic keys

Pablo G贸mez ochoa Iv谩n SoSa SamPer

3D images anD augmenteD reality

Author: Pablo G贸mez Ochoa e Iv谩n Sosa Samper.

Format: 22 x 28 cm.

Number of pages: 88.

Number of images: 39 3D ilustrations.

120-150 photographies.

Binding: Hardcover, wire-o.

RETAIL PRICE

85

This is a pioneering book in veterinary medicine. The reader will be able

ebook

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to visualise what really is happening in a diseased heart. Through threedimensional representation and augmented reality, every disorder can be seen, almost touching the 3D model above the book. In addition, the changes in blood flow produced by the pathologies can be visualised, bringing the reader even closer to the pathophysiological reality.

The text addresses the major points of pathophysiology and diagnostic keys for the most common diseases, and the illustrations and pictures are a bridge between the 3D models and the text. Thus, the book succeeds in joining diagnosis, and particularly a test such as echocardiography, with the understanding of the pathophysiology.

Presentation of the book Since I started learning echocardiography, I translated what I saw on the screen, along with the findings of the X-ray and the ECG, into an internal three-dimensional model that I used to create a comprehensive picture of the clinical condition of the patient. Being able to see it now, throbbing in front of me, generates endless emotions. The first and most important, is the play instinct. I try to stroke it with my extended fingers, I try to penetrate it from the pulmonary vein and I turn and bend the sheet watching the model changes with a giggle. I think any creative idea that materialises is cause for celebration, but for me, the design of this heart and being able to see it beating thanks to Pixeldreams modelling and the support of Grupo As铆s is a unique moment. However, the same question is repeated from the moment I see this heart beating: will this model, together with the text and illustrations, teach anything? We will see whether augmented reality is as an artifice in the history of technology or whether it really represents a change in the way we teach. I believe that a material with soul and passion always transmits something. So my bet is that this book will make the reader internalise the pathology, visualising the pathophysiology and overcoming the hurdle that the study from two-dimensional media, such as photographs of X-rays or ultrasounds, represents.

Pablo G贸mez

3D Cardiology in small animals:

The authors Pablo G贸mez Ochoa He graduated from the University of Zaragoza in 2000, and completed his PhD at the same institution in 2004. He obtained a national and an international award for his PhD research, and has published over 20 scientific articles in international journals. He has been a speaker at over 50 CE courses, and national and international conferences.

He has done external rotations on ultrasonography in human hospitals, and in the Animal Health Trust. In 2006, he was a Visiting Professor at The Ohio State University and Kansas State University Colleges of Veterinary Medicine. In 2010 he was a Visiting Professor at the Universita di Sassari in Italy. In his field, Dr G贸mez Ochoa developed a technique utilising contrast material to identify portosystemic shunts, and adapted the use of semiquantitative Doppler studies to evaluate intraabdominal lymphadenopathy.

He is currently Professor, part-time, at the University of Zaragoza, and is researching novel contrast agents and additional application of Doppler in various clinical conditions. In 2012 he co-founded Vetoclock.com with Guillermo Couto.

Ivรกn Sosa Samper He obtained his DVM degree in 2007 from the University of Zaragoza. He worked for a year in a small animal practice in Valencia while at the same time offering mobile ultrasound services to other veterinary clinics. He later worked for a year in a small animal hospital in Oxford, UK, in the Cardiology and Ultrasound Department. In 2009, he completed a Small Animal internship at Bristol University, working then in the Cardiology department of the university and as a sonographer at Great Western Referrals, centre of excellence in Swindon, UK. He has published science articles and communications in national and international conferences, and participated in ultrasonography courses in Spain and the UK. Since 2012, Ivรกn started a combined cardiology residency PhD programme. His research topic involves stem cell and resynchronisation therapy in dilated cardiomyopathy.

3D Cardiology in small animals:

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3D Cardiology in small animals Pathophysiological and diagnostic key concepts

Pablo G贸mez ochoa Iv谩n SoSa SamPer

3D images anD augmenteD reality

Table of contents Introduction Normal heart Longitudinal section Three-dimensional anatomy and sonographic correlation Pathophysiology of heart failure Cardiac remodelling. Pressure overload Volume overload

Acquired heart diseases Myxomatous mitral valve disease Canine dilated cardiomyopathy Feline hypertrophic cardiomyopathy Endocarditis Feline restrictive and unclassified cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy Cardiac neoplasms Pericardial effusion and cardiac tamponade

Congenital heart diseases Patent ductus arteriosus (PDA) Patent and reversed ductus arteriosus Pulmonic stenosis Aortic stenosis Ventricular septal defect (VSD) Tricuspid dysplasia and Ebstein’s anomaly Mitral dysplasia Tetralogy of Fallot Atrial septal defect Peritoneopericardial diaphragmatic hernia

Normal heart Canine external heart view

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External heart RP long-axis with left ventricular outflow tract 6

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3D Cardiology Introduction Three-dimensional structure, haemodynamics and pressure gradients Traditional Cardiology teaching claimed that the heart consists of four chambers: two atria and two ventricles. However, this view has changed since the 70s, when Cardiologist Torrent Guasp described his myocardial band theory. The ventricular myocardium consist of a single band, extending from the pulmonary artery to the aorta, that turns and twists in a helix thus forming both ventricles. Thanks to this model some of the key points of cardiac performance can be explained.

First of all, the heart is not just an ejection pump, it is also a suction pump that during diastole —thanks to the separation of the atrioventricular valve annulus and the apex— manages to aspirate blood from the atria to the ventricles. Furthermore, energy consumption by the heart having been proved, diastole is no longer considered a passive relaxation phase.

Shape and position of the canine heart in the chest.

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Cranial vena cava Brachiocephalic trunk Subclavian artery Aorta Right pulmonary artery

The second important point this model explains is the existence of two hearts locked within the heart, that keep the blood flowing through two different circuits: a highpressure one —the left one—, and a high-capacity lowpressure one —the right one. For each systole, the right ventricle and the left ventricle ejection volumes in a healthy animal are the same. Thus, all the volume on the right side goes to the lungs, keeping a low pressure by means of a high capacity (20 mmHg), while the volume in the left circuit is distributed among all organs (except the heart, myocardial perfusion occurring during diastole) maintaining a high pressure (120 mmHg).

The third distinctive feature of this model is the concept of haemoskeleton, which considers the blood as an interface that, thanks to its viscous fluid properties, provides support to the band facilitating its expelling pump function and originating the axial flow (blood column in motion) and radial flow (pulse wave).

Shape and position of the canine heart in the chest.

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Ligamentum arteriosum Left pulmonary artery Pulmonary trunk Pulmonary vein Caudal vena cava

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Three-dimensional anatomy and sonographic correlation

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3D Cardiology Introduction This book presents the main heart diseases in augmented reality. It shows the full heart and the changes that occur, as well as different views of the various pathologies. This chapter is intended as a guide that the reader can consult when reviewing the diseases or their ultrasound images, in order to remember the correlation between the ultrasound image and its 3D equivalent.

Echocardiography was a significant breakthrough in the world of Cardiology. The possibility to dynamically explore the heart chambers and valves, as well as blood flow, with the introduction of Doppler ultrasound, was a true revolution. While this dynamism may not be reflected in an image, it must be remembered that echocardiography is not a piano, but a trombone, which not only consists of the representation of standard views.

Cutting the heart along its long axis (longitudinal plane), exploration begins on the right side. To toggle between this view and the next you just have to slightly change the angle of the probe wherein a cross section of the left ventricle outflow tract and the right branch of the pulmonary artery is displayed. The name of this plan is right parasternal long-axis of the left ventricular outflow tract. Then,

rotating the probe by 90째, the longitudinal plane changes to transverse. The heart is scanned by sections from the apex to the cardiac base. The probe swings from an almost parallel to the sternum location towards the armpit. The first view is at papillary muscle level, and is called right parasternal short-axis. After this view, the chordae tendineae and then the mitral valve are displayed by slightly angling the probe towards the armpit. The latest views from the right side are the right parasternal short-axis views at the level of the base of the heart.

In the first one, the level of the view is the aortic valve which, with its three valves, has the shape of a threeleafed clover when closed during diastole. In this plane, and with the valve closed, the ratio left atrium/aorta can be measured. The next view, right parasternal short-axis right outflow tract can be obtained with a slight angle of the probe from its previous position. It shows the left atrium, the pulmonary valve and the artery bifurcation.

In this plane, the right heart embraces the aorta; the right atrium, the tricuspid valve, the right ventricle and the pulmonary artery can be seen. This is the end point of the right side of the animal views.

To interpret the scans compared to the 3D model it should be remembered that the marker of the probe corresponds to the red circle on the ultrasound image. Right parasternal long-axis four-chamber view.

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Myxomatous mitral valve disease Longitudinal view of a myxomatous degeneration

External heart RP long-axis with left outflow tract / RP short-axis papillary muscles / RP short-axis at the base of the heart 22

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3D Acquired Cardiology heart diseases Description and pathophysiology Chronic valvular disease (CVD), Mitral endocardiosis or Myxomatous Mitral valve degeneration, is the most common acquired heart disease in dogs. Ten percent of animals presenting to the practice is estimated to have heart disease, and 75 % of these animals have degenerative mitral valve disease. Thirty percent of patients will also show degenerative lesions of the tricuspid valve. In terms of epidemiology, it is worth noting its prevalence in males (1.5 times more frequently than in females) and increased prevalence in small breeds, although this condition is also seen in large breed dogs. The progression of the disease is completely unpredictable, although large breed dogs usually show a faster progression. The onset of the disease is linked to a systolic murmur of mitral regurgitation, which can take years to precipitate haemodynamic instability and, consequently, clinical signs and congestive heart failure. There is some breed predisposition, especially in the Cavalier King Charles Spaniel, showing an earlier onset of the disease, although its progression does not seem to be different from that in any other small breed dog. The prevalence of CVD increases with age in dogs under 20 kg (85 % of 13-year old small dogs show some degree of valvular lesion at necropsy).

The cause of this condition is unknown, but a hereditary component has been demonstrated in several breeds.

Changes in the valve affect both the extracellular matrix and the cells of the valve apparatus (valves and chordae

Volume overload and secondary pulmonary congestion leading to a pressure increase in the circuit.

tendineae). Both the endothelium and subendothelium thicken, although an increase in thromboembolic disease or endocarditis has not been proved. As the disease progresses, valve prolapse and ruptured chordae are common occurrences that worsen the prognosis. Disease progression leads to increased heart workload and remodelling with eccentric hypertrophy, which over time may lead to systolic dysfunction. The literature describes an abnormal number of receptors for serotonin, endothelin and angiotensin in these stages, as well as fibroblasts, which in all likelihood plays a crucial role in the pathophysiology of the disease. Neurohormonal and inflammatory mediators have also a major impact, although their role in the development of the disease is not completely understood.

Although aetiology or conditioning factors that affect the progression of the disease are still vague, it is known that age, left atrial size and heart rate are prognostic factors.

Diagnostic keys The diagnosis of CVD is based on the auscultation of a left apical murmur. Dogs may show clinical signs of congestive heart failure: tachypnoea, dyspnoea, exercise intolerance, coughing, or syncope. The diagnostic guidelines of the American College of Cardiology allow the veterinary surgeon to classify dogs depending on their pathophysiological stage. Animals in phase A include predisposed breeds, such as Cavalier King Charles Spaniel, with no murmur.

The veterinary surgeon should warn the owner about the breed predisposition, and recommend an annual auscultation. Animals in phase B include animals with a murmur but without clinical signs. A complete diagnostic evaluation including X-rays, ECG, blood pressure measurements, blood tests with electrolytes and echocardiography is recommended. This constitutes a good baseline assessment for subsequent follow-ups. Phase B can be broken down into two sub-phases, B1 and B2, in which we find asymptomatic dogs with a murmur but without haemodynamic effects (B1) and asymptomatic dogs with a murmur, and with evident cardiac remodelling (B2). Although X-rays and ECGs are useful to identify cardiomegaly, echocardiography determines whether regurgitation has a haemodynamic effect and is able to define remodelling before the previous two. The measurements and indices typically assessed to include an animal in the B2 group are: left atrium/aorta ratio, in the right parasternal short-axis view at the base of the heart; assessment of diastolic function in left apical views; and mitral regurgitation Doppler study.

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Arrhythmogenic right ventricular cardiomyopathy Biventricular and biatrial enlargement

External heart RP long-axis with ventricular premature beat 38

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3D Acquired Cardiology heart diseases Description and pathophysiology Arrhythmogenic right ventricular cardiomyopathy is a disease of the myocardium to which Boxer dogs are specially predisposed. A genetic basis and an autosomal dominant transmission with incomplete penetrance have been identified.

Its pathophysiology is characterised by an alteration in the conduction system of the right ventricle due to the replacement of myocardial cells with fibrosis or fat. The disease may either remain concealed (with the generation of premature ventricular complexes), present with arrhythmogenesis and clinical signs, or evolve into a form with arrhythmias and congestive heart failure.

premature complexes. If any are found, an echocardiography must be considered to assess cardiac morphology and function. However, ECG and the Holter monitor are the most useful tools in early diagnosis. Premature ventricular complexes with a left bundle branch block morphology in lead II, and ventricular tachyarrhythmias can be found in the electrical study. A normal ECG or Holter does not exclude the possibility of developing the disease.

Diagnostic keys The clinical signs are very different depending on the clinical manifestation of the disease. Syncope, fatigue, and ascites occur in animals with arrhythmogenic right ventricular cardiomyopathy with congestive heart failure. However, quite often dogs with arrhythmias or with the concealed form present no clinical signs or, if they do, these are in the form of syncope. This is one of the diseases that can cause sudden death without previous clinical manifestations.

The only available tool against this disease is early diagnosis. It is advisable to carry out annual examinations of Boxer dogs in order to investigate the presence of

Arrhythmogenic right cardiomyopathy in a 5-year-old Boxer. Although it is not the most common finding, a marked biventricular enlargement was observed in this case.

Premature ventricular complex with a left bundle branch block morphology, which points to a right ventricle origin.

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Patent ductus arteriosus (PDA) Ductal ampulla in enlarged pulmonary artery

External heart RP long-axis with left outflow tract / Left cranial pulmonary artery / RP short-axis at the base of the heart right outflow tract 48

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3DCongenital Cardiology heart diseases Description and pathophysiology Patent ductus arteriosus (PDA) is, along with aortic stenosis and pulmonic stenosis, one of the most common congenital heart defects in dogs. However, it is rare in cats and is often associated with other diseases. There is a significant gender predisposition (where females outnumber males by 3 to 1) and breed predisposition (German Shepherd, Yorkshire Terrier, Bichon Maltese, Pomeranian, and others) in this condition. Patent ductus arteriosus is the persistence of the sixth aortic arch, and it allows blood to bypass the foetus pulmonary circulation, thus protecting the immature lungs against circulatory overload. The lack of smooth muscle is the cause of this persistence, preventing the ductus from closing after birth. Several types of PDA have been described depending on its distribution. The greater the lack of musculature, the larger the ductus is, and the more blood passes through it.

Its pathophysiological evolution depends on the amount of blood that passes through the ductus, causing volume overload, and the pulmonary circuit response

to this overload. As the pressure in the aorta is higher in both systole and diastole, blood goes into the pulmonary artery throughout the cardiac cycle; thus, the pulmonary artery collects the blood that the right ventricle ejects plus the blood that goes through the ductus. This entire blood volume passes through the lungs and causes an overload in the left atrium and left ventricle which leads to their enlargement. In many animals it is common for the mitral annulus to become enlarged, generating a reflux that can cause lung congestion and even congestive heart failure. Chronic volume overload may lead to systolic dysfunction and atrial fibrillation, when the atrium reaches sufficient mass. If the amount of blood does not generate significant damage to the pulmonary circuit, the blood will continue flowing from left to right; but if the tunica intima of the pulmonary arteries gets damaged and proliferates, or if traces of foetal circulation remain, reversal of blood flow and pulmonary hypertension will result, provided that the pressure within the pulmonary system exceeds the pressure of the systemic circulation.

Colour Doppler showing the turbulence in the pulmonary artery caused by the ductus arteriosus.

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Pulmonic stenosis Leaflet fusion and post-stenotic dilation

External heart RP short-axis base of the heart with right outflow tract / Left cranial pulmonary artery / RP short-axis papillary muscles 56

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3DCongenital Cardiology heart diseases Description and pathophysiology Pulmonic stenosis is one of the most common congenital defects in dogs. However, it is rare in cats and is often associated with other abnormalities. It is important to know the breeds that are predisposed to this condition, which include the French Bulldog, English Bulldog, Yorkshire Terrier, West Highland White Terrier, Boxer, Miniature Schnauzer, Cocker Spaniel and Samoyed. Furthermore, breeding studies have demonstrated a pattern of autosomal dominant inheritance in Beagles and Keeshounds.

The key points in the development of this disease include an increased systolic pressure in the right ventricle, and the presence or absence of tricuspid regurgitation.

Right ventricular pressure increases due to flow obstruction. The most common type of pulmonic stenosis is due to the fusion of the leaflets of the pulmonic valve, type A. Post-stenotic dilation of the main pulmonary artery is common in this type of stenosis. In some cases, the pulmonary annulus is hypoplastic (type B) with little or no post-stenotic enlargement.

Subvalvular stenosis are less common and are usually secondary to the valvular stenosis, or due to the presence of a fibrous band in the infundibulum, or a fibrobuscular band, termed double-chambered right ventricle.

Right ventricular hypertrophy caused by pressure overload in the right ventricle.

Finally, supravalvular stenosis are caused by the presence of a membrane in the pulmonary artery, or the narrowing of this artery or one of its branches. Supravalvular pulmonic stenosis is rare and has been described in the Giant Schnauzer.

The pathophysiologic mechanism is the same regardless of the type of stenosis. Ventricular systolic pressure increases with the obstruction, generating turbulent flow that, in case of valve stenosis, generates a post-stenotic dilation. The right ventricle responds to this pressure increase with concentric hypertrophy that remodels and changes the cardiac geometry. Consequently, and depending on the degree of hypertrophy generated, the infundibulum itself can obstruct the blood outflow through the pulmonary artery (dynamic obstruction). In addition, right ventricular hypertrophy and dilation can lead to a coaptation failure of the tricuspid valve with increased diastolic pressure. Tricuspid regurgitation secondary to a ventricular geometry change can lead to congestive right heart failure. This failure is not acquired in 10-20 % of dogs, but due to some existing degree of tricuspid dysplasia.

Severe hypertrophy leads to poor myocardial oxygenation, arrhythmogenesis and the development of ventricular hypocontractility and reduced cardiac output.

The flow obstruction caused by the stenosis increases the pressure in the right ventricle, resulting in hypertrophy in an attempt to control the wall stress.

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E-book

3D Cardiology in small animals

Pathophysiological basis and diagnostic keys

Digital version

Augmented reality

3D videos of the main heart diseases VIdeo Heart function

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