
- •Preface
- •Acknowledgments
- •Basic Physics
- •Transducers and Resolution
- •Doppler Physics
- •Artifacts
- •Summary
- •Introduction
- •Patient Preparation
- •Patient Positioning
- •Transducer Selection
- •Two-Dimensional Images
- •Two-Dimensional Imaging Controls
- •Introduction
- •M-Mode Echocardiography
- •Color-Flow Doppler
- •Spectral Doppler
- •Tissue Doppler Imaging
- •Measurement and Assessment of Two-Dimensional Images
- •Measurement and Assessment of M-Mode Images
- •Measurement and Assessment of Spectral Doppler Flow
- •Measurement and Assessment of Tissue Doppler Imaging
- •Evaluation of Color-Flow Doppler
- •Evaluation of Ventricular Function
- •Mitral Regurgitation
- •Aortic Regurgitation
- •Tricuspid Regurgitation
- •Pulmonary Regurgitation
- •Endocarditis
- •Pulmonary Hypertension
- •Systemic Hypertension
- •Hypertrophic Cardiomyopathy
- •Dynamic Right Ventricular Outflow Obstruction
- •Moderator Bands
- •Dilated Cardiomyopathy
- •Right Ventricular Cardiomyopathy
- •Restrictive Cardiomyopathy
- •Endocardial Fibroelastosis
- •Arrhythmogenic Right Ventricular Cardiomyopathy
- •Myocardial Infarction
- •Myocardial Contusions
- •Pericardial Effusion
- •Neoplasia as a Cause of Pericardial Effusion
- •Pericardial Disease
- •Abscesses
- •Pericardial Cysts
- •Thrombus
- •Ventricular Septal Defect
- •Patent Ductus Arteriosus
- •Aorticopulmonary Window
- •Right to Left Shunting PDA
- •Atrial Septal Defects
- •Endocardial Cushion Defects
- •Bubble Studies
- •Atrioventricular Valve Dysplasia
- •Outflow Obstructions
- •Inflow Obstructions
- •Tetralogy of Fallot
- •APPENDIX ONE Bovine
- •APPENDIX TWO Canine
- •APPENDIX THREE Equine
- •APPENDIX FOUR Feline
- •APPENDIX FIVE Miscellaneous Species
- •Index
associated with pulmonary hypertension are seen including severe right ventricular hypertrophy and a very prominent pulmonary artery. Chapters 4 and 6 describe the findings of pulmonary hypertension. Doppler flow will be negative when the shunt is interrogated on right parasternal four-chamber views. Aortic flow velocities will be elevated since the shunt now involves that vessel.
Endocardial Cushion Defects
When both a very large ostium primum atrial septal defect and a large ventricular septal defect are present, the abnormality is called an endocardial cushion defect. It may also be called complete atrioventricular canal or atrioventricular septal defect (62,100,101). Endocardial cushion defects fall into two categories: incomplete (or partial) and complete. Complete defects include an ostium primum atrial septal defect and a ventricular septal defect where a large portion of the inferior atrial septum and a large portion of the superior portion of the ventricular septum are missing. These two septal defects connect and the entire central portion of the heart is missing. There is typically one large atrioventricular valve since the septal portion of the endocardial cushion did not develop sufficiently to form the septal portions of the AV annuluses. Incomplete endocardial cushion defects involve a very large ostium primum atrial septal defect resulting in an almost common atrium and abnormalities of the atrioventricular valves (1,100) (Figure 9.29). The mitral valve is often cleft (1,100).
Two-dimensional echocardiographic images are very dramatic. The right parasternal four-chamber view shows a large atrial septal defect as well as the ventricular septal defect (Figure 9.34). The mitral and tricuspid valves originate from the endocardial cushion and are usually dysplastic. There often appears to be just one large atrioventricular valve with only the parietal leaflets of the tricuspid and mitral valves present. When septal mitral and tricuspid leaflets are present, they are usually continuous through the endocardial cushion defect. The right atrium, right ventricle, and left atrium are always dilated. The left ventricle may be dilated. The valves are usually insufficient, and the defects are so large that both color-flow and spectral Doppler are of no help in determining the direction of flow.
Figure 9.34 Endocardial cushion defects have a large ostium primum atrial septal defect and a ventricular septal defect. (A) Long-axis four-chamber images show large portions of both the atrial and ventricular septums missing. Only the parietal leaflets of the mitral and tricuspid valves are present. (B) Transverse views of the heart base show the large ostium primum defect of this endocardial cushion defect (arrow). (C) Transverse images at the level of the left ventricle show the large ventricular septal defect associated with the endocardial cushion defect (arrow). AO = aorta, RA = right atrium, LA = left atrium, RV = right ventricle, LV = left ventricle, IAS = interatrial septum.

Bubble Studies

Bubble studies help confirm the existence of right to left shunting. Normal saline is drawn into a syringe, shaken vigorously, all large bubbles of air are pushed from the syringe leaving only microbubbles within the solution. Several milliliters of saline are used in larger dogs, but about 1 milliliter is used in cats and other small animals. The saline is injected into a peripheral vein while the heart is being imaged. A right parasternal four-chamber view is used for the detection of atrial septal defects, and a right parasternal long-axis left ventricular outflow view should be used for ventricular septal defects. Dense echoes associated with the air-filled fluid can be seen crossing the atrial or ventricular septums into the left-sided chambers (62,102,103).
Bubble studies
help identify R → L shunts
use the abdominal aorta for PDA
Because the shunt in patent ductus arteriosus is extracardiac and blood flows from the pulmonary artery into the descending aorta, a bubble study using cardiac images will not help define the existence of a reverse PDA. The abdominal aorta should be used instead (Figure 9.35). The dense echoes associated with the microbubbles will show up in the abdominal aorta if a reverse PDA exists (92). It is important to rule out VSD and ASD since these reverse flows will also be seen in the abdominal aorta (103).
Figure 9.35 (A) The abdominal aorta is examined when performing a bubble study to confirm the presence of reverse patent ductus arteriosus. (B) Dense echoes associated with reverse flow (arrows) fill the aorta if a reverse shunt of any kind is present. A bubble study within the heart rules out reversed atrial or ventricular septal defects. These will also cause bubbles to appear in the abdominal aorta. AO = aorta.

Atrioventricular Valve Dysplasia
Congenital dysplasia of the atrioventricular valves usually causes valvular insufficiency. The degree of dysplasia and regurgitation is very variable. The cardiac changes associated with these defects are similar to those seen when the valvular insufficiencies are secondary to acquired valvular lesions. Cardiac changes associated with mitral dysplasia include and eccentric left ventricular hypertrophy, elevated parameters of left ventricular function, left atrial dilation, and excessive wall and septal motion (62). Right-sided changes associated with tricuspid dysplasia include right ventricular volume overload, possible paradoxical septal motion, and right atrial dilation (62). For details and further description of these changes, refer to Chapter 5 and the discussions on acquired mitral and tricuspid valve disease. Descriptions of the two-dimensional appearance of the dysplastic atrioventricular valves follow.
The appearance of the valvular apparatus is extremely variable, and any combination of abnormally shaped leaflets, abnormal chordal attachments, and abnormal papillary muscles may be seen. The leaflets may be thick, long, short, contain clefts, or have some degree of commissural fusion. The papillary muscles may be abnormally shaped or elongated or large (54,57,60).
Tricuspid Dysplasia
This defect of the tricuspid valve is particularly common in Labrador retrievers, but other large breed dogs are also predisposed to the defect (54). The septal leaflet is typically tethered to the right side of the septum. Short chordae may be visible as the leaflet tries to move toward its normal closed position during systole (Figure 9.36). The middle of the leaflet often buckles away from the septum while the tips remain closely apposed to the septum. The anterior leaflet is typically elongated and may come close to achieving closure of the tricuspid valves during systole. It is sometimes difficult to define where the anterior leaflet of the tricuspid valve ends and where the chordae tendinae start (21).
Figure 9.36 Tricuspid dysplasia may involve any aspect of the tricuspid apparatus. Typically, the septal leaflet of the valve is tethered to the interventricular septum by short chordae. Often the parietal tricuspid valve leaflet is elongated with abnormal attachment to a web of papillary muscles. (A) The septal leaflet is seen tethered to the septum (small arrow). Notice that the mitral leaflets are closed while the tricuspid leaflets are wide open. There is abnormal papillary muscle architecture (long arrows) at the apex of the right ventricle. (B) The web of papillary muscles at the apex of the right ventricle is seen here (short arrow), and there is a glimpse of the septal leaflet as it remains tethered to the septum (long arrow). (C) The tricuspid valve leaflets in this dog have chordae that attach abnormally to the leaflets (arrows). Planes = right parasternal four-chamber views, RV = right ventricle, RA = right atrium, LV = left ventricle, LA = left atrium.

An unusual variation of tricuspid dysplasia is Ebstein’s Anomaly. The tricuspid annulus is actually displaced toward the apex of the right ventricle (104). The right atrial chamber is very large in this

defect, and the ventricle is called atrialized. The annulus can be identified on right parasternal longaxis four-chamber views of the heart. The mitral and tricuspid annulus should be aligned almost directly across from each other in normal hearts. The tricuspid valve is typically a millimeter or 2 closer to the apex of the normal heart than the mitral annulus. With Ebstein’s anomaly, the tricuspid annulus is clearly displaced toward the apex (Figure 9.37). Be sure to examine the septal cusp carefully since a severely tethered leaflet may only move away from the septum at a more apical location and yield the appearance of a displaced annulus. Regardless, the valve is dysplastic (21).
Figure 9.37 With Ebstein’s anomaly, the tricuspid annulus is displaced toward the apex of the right ventricle. (A) An atrialized right ventricle is seen with tricuspid annular displacement to the apex (small arrow). The normal point of attachment should be at the level of mitral annulus (large arrow). (B) The tricuspid annulus (long arrow) is situated closer to the apex of the right ventricle compared to the mitral annulus (short arrow). This image also shows evidence of a patent foramen ovale (thick arrow).
Even though the right atrium is enlarged because the leaflets close in a more apical location than normal, tricuspid insufficiency is not always severe. Often valves with very abnormal architecture on
echocardiographic images are only mild to moderately incompetent.
Mitral Dysplasia
Mitral dysplasia is particularly common in cats (60). As with tricuspid dysplasia, the leaflets may be short and thick or elongated. They may be associated with abnormally shaped, elongated or large papillary muscles, and aberrant chordae tendinae with abnormal attachments to the ventricular wall or septum (Figure 9.38). Although it does occur, the septal leaflet is not usually tethered to the septum as in tricuspid dysplasia. The valves may display increased echogenicity and abnormal motion secondary to malformation of the mitral apparatus. There may be prolapse and some degree of restricted motion secondary to commissural fusion or abnormal chordae tendinae (54,57).
Figure 9.38 Mitral dysplasia is associated with abnormally shaped, elongated, or large papillary muscles and aberrant chordae tendinae with abnormal attachments to the ventricular wall or septum. (A) Aberrant chordae tendinae (arrows) with abnormal attachments to the ventricular wall are present in this cat. Plane = right parasternal transverse mitral valve. (B) Chordae tendinae extend from the papillary muscles to the septum and lateral wall (arrows) of the left ventricular chamber in this cat. Plane = right parasternal transverse left ventricle. (C) Abnormal muscular protrusions from the septum and aberrant chordae tendinae with attachments to the ventricular wall are present in this cat. Plane = right parasternal left ventricular outflow view. (D) This dog has abnormal points of mitral chordal attachment (arrows) to the lateral wall of the ventricular chamber. Plane = right parasternal transverse mitral valve, VS = ventricular septum, LV = left ventricle, AO = aorta, LA = left atrium, RV = right ventricle.


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CHAPTER TEN
Stenotic Lesions
Outflow obstructions created by aortic or pulmonary stenosis create excessive work for the ventricles and lead to concentric hypertrophy of the respective chamber. The hypertrophy develops in order to normalize systolic wall stress (1,2). Pulmonary stenosis leads to hypertrophy of both the right ventricular wall and the septum, while aortic stenosis leads to increased free wall and septal thicknesses. The chamber size may be smaller than normal secondary to the hypertrophy. Mild obstructions to outflow may not result in any visible changes within the heart, and Doppler studies are necessary to confirm the presence of mild stenosis on either side of the heart.
Inflow obstruction secondary to mitral and tricuspid stenosis is much less common. The resistance to filling of the ventricular chambers results in dilated atria. The atrioventricular valves are often incompetent as well. Obstructions can also exist within the atrial chambers and will create the same hemodynamic problems as valvular stenosis.
The many varying morphological manifestations of these stenotic lesions are presented here. An algorithm has been created that provides the echocardiographer with specific parameters that logically lead to a diagnosis and assessment of severity in animals with isolated congenital heart defects (Figure 10.1) (3). This algorithm works well when the congenital heart disease is not complicated with other concurrent cardiac problems such as valvular insufficiency, pulmonary hypertension, or combinations of stenotic or shunt lesions.
Figure 10.1 Echocardiographic algorithm for the evaluation of canine congenital heart disease.
Reprinted with permission of Oyama MA, Sisson DD. Evaluation of canine congenital heart disease using an echocardiographic algorithm. J Am Anim Hosp Assoc 2001;37:519–535.