Physical Examination

Physical examination of the cardiovascular system involves examination of mucous membranes for color, refill time, and moistness; thoracic palpation and auscultation, assessment of arterial pulse quality via the median or medial saphenous arteries; assessment of jugular filling; and palpation of the ventrum for edema. Common ancillary tests include blood analysis, blood pressure measurement, thoracic radiography, electrocardiography, and echocardiography. The areas suitable for cardiac auscultation lie conveniently within the short-fleeced axilla, under the forelimb above the elbow. On the left side, the pulmonic valve is heard best over the third intercostal space, under the triceps brachii, whereas the aortic valve area is located more dorsally at the fourth intercostal space. The mitral valve area is located more ventrally on the left hemithorax at the costochondral junctions over the fourth or fifth intercostal space, and the tricuspid valve is heard best on the right hemithorax over the fourth intercostal space at the caudal edge of the triceps brachii. Areas over all valves should be palpated for the presence of a thrill. Healthy adult camelids in the Oregon State University herd have resting heart rates between 48 and 72 beats per minute (beats/min), with rare individuals spiking up to 84 beats/min. This range is slightly lower than the 60 to 90 beats/min or higher rates that are sometimes cited. Adults with higher heart rates are likely to be excessively stressed, volume depleted, or otherwise compromised. Neonates typically have heart rates varying from 90 to 120 beats/min, although rates up to 140 beats/min may be found in some newborns. Juveniles typically will have heart rates less than 100 beats/min by age 1 month, and this declines to the adult range by age 1 year.¹

The first and second heart sounds should be heard clearly on the left side of the thorax in all but the most obese camelids. These sounds are more difficult to discern on the right side but should be audible in an adequately restrained camelid in a quiet environment. With careful auscultation, soft third and fourth sounds are discernible in some healthy camelids. Loud S3 or S4 heart sounds are usually indicative of serious cardiac disease, reflecting the presence of ventricular enlargement and ventricular dysfunction. Physiologic and innocent murmurs are often identified in adult and immature camelids. Anemic, systemically ill, and even apparently healthy camelids may exhibit soft, nonpathologic systolic murmurs (≤grade 3 of 6) over the left heart base. These murmurs are usually crescendo–decrescendo, ejection-type murmurs occupying midsystole, with preservation of the first and second heart sounds. Scansen and co-workers recently identified high-velocity and turbulent flow in the branch pulmonary arteries of several young crias and offered an elegant explanation for some of the innocent murmurs identified in immature camelids.² The murmur and the flow disturbances resolved within a few months, which suggests that this finding is benign, therein resembling the condition of peripheral pulmonary stenosis seen in human infants. Often, however, the precise cause of these soft murmurs is not apparent even with the aid of color flow echocardiographic evaluation.

Loud systolic murmurs are abnormal and may be detected in camelids with septal defects, outflow tract obstructions, and insufficiency of the atrioventricular (AV) valves. The systolic murmur of a ventricular septal defect may be either band shaped or crescendo–decrescendo and is typically best heard on the right side of the chest. Heart murmurs resulting from outflow tract obstruction are typically crescendo–decrescendo or diamond-shaped and are usually best heard at the left heart base. The regurgitant murmurs of AV valve insufficiency are typically band shaped or plateau shaped and are best heard at the left or right apex, depending on the valve affected. Regurgitant murmurs tend to be longer (pansystolic) than systolic ejection murmurs (holosystolic), so both the first and second heart sounds are usually obscured in camelids with AV valve insufficiency. In comparison with horses and dogs, insufficiency of the AV valves occurs much less commonly in llamas and alpacas. Diastolic murmurs are also relatively rare, almost always clinically significant, and are usually caused by insufficiency of the aortic valve, or more rarely, the pulmonic valve. Such murmurs are usually best heard at the heart base on the left side of the thorax. The continuous murmur of a posterior descending artery (PDA) is also best heard at the left heart base as in other species. It is important to recognize that many significant congenital and acquired cardiac lesions in camelids result in no discernible murmur. For example, camelids with a large ventricular septal defect (VSD) and pulmonary hypertension may not evidence a murmur but will often have accentuated splitting of the second heart sound because of asynchronous closure of the semilunar valves. Thus, it must be appreciated that auscultation alone is not entirely reliable for ruling out the presence of cardiac disease.

The lymphatic system is often conveniently assessed by examining the size of peripheral lymph nodes, particularly when they are enlarged because of inflammation or neoplasia. Moreover, it is not uncommon to identify disorders of the lymphatic system by inference when lymph accumulates in a body cavity or regional pitting is noted in an extremity. The easiest lymph nodes to find in normal camelids include the prescapular nodes located near the base of the neck and the superficial inguinal nodes located in the inguinal region close to the ventral body wall. Other peripheral nodes are difficult to locate in healthy camelids because they often comprise a collection of small nodules. Emaciation or pathologic node enlargement facilitates successful palpation of the submandibular, retropharyngeal, and popliteal nodes, which are often very hard to identify in healthy animals.

Electrocardiography

Electrocardiograms (ECGs) are primarily recorded to elucidate the nature of an auscultated rhythm disturbance. A standardized six-lead ECG may be easily obtained in the standing camelid by attaching two electrodes above the olecranon on the forelimbs and the remaining two electrodes just above the patellas on the hindlimbs. Leads are attached with alligator clips and wetted with alcohol. Clipping the fleece is usually not necessary. It is often preferable to obtain ECGs in young crias by restraining them in right lateral recumbency. In either circumstance, ECG tracings are most easily interpreted when a paper speed of 50 millimeters per second (mm/s) is selected for the recording. It is useful to complement the limb leads with a rhythm strip that is recorded by using a base–apex lead; the rhythm strip is obtained by repositioning the right front leg electrode to the base of the neck on the right and by moving the left front leg electrode to a location over the cardiac apex on the left side of the chest. This lead often provides the largest amplitude complexes thereby facilitating cardiac rhythm analysis.³

Normal ECG reference values for camelids have been reported in several published studies (Figure 36-1).^4–6 In the recent report by Kraus and coworkers, heart rate was seen to vary from 60 to 100 beats/min with a mean heart rate of 80 beats/min.⁶ The mean (+/− standard deviation [SD]) duration of the electrical events were reported as follows: P waves: −40 milliseconds (ms; +/− 12); PQ interval: 150 ms (+/− 33); QRS complex: 50 ms (+/− 8); Q–T interval: 360 ms (+/− 60); ST segment: 230 ms (+/− 46). QRS morphology was found to be extremely variable. The mean polarity of the QRS complexes was negative in 60% of the lead I recordings, in 56% of the lead II recordings, and in 51% of the lead III recordings. The QRS complex was least variable for lead V10, where the QRS complexes were positive in 88% of the animals examined. The amplitudes of the R and S waves tended to be low in the limb leads, as often noted in herbivores. Values obtained from mean electrical axis (MEA) estimations were extremely variable but were directed mainly to the right and in a cranial direction. In contrast to humans and small animals, ECG recordings obtained from camelids provide little information about the overall size of the heart or the enlargement of specific chambers. The Purkinje fiber network of camelids penetrates completely through the wall of the ventricles from the endocardium to the epicardium, as in sheep, resulting in a pattern of activation that effectively obscures the hallmarks of chamber enlargement seen in humans and smaller mammals such as the dog and the cat.^4,7 In our experience, neither the recorded voltage nor the estimated MEA appears to be useful for the detection of chamber enlargement.

Cardiac rhythms observed in healthy camelids include sinus rhythm and, more commonly, sinus arrhythmia with an occasional animal showing first or low grade second-degree heart block, presumably as a result of high vagal tone. In anxious animals, an occasional premature supraventricular beat may also be noted.⁴ With the exception of sinus bradycardia and sinus tachycardia, cardiac arrhythmias and conduction disturbances are infrequently detected in camelid species. However, a variety of rhythm disturbances are occasionally observed in animals that are experiencing environmental adversity, are systemically ill, or have serious underlying congenital or acquired heart disease. Observed rhythm disturbances include premature atrial and ventricular depolarizations, supraventricular and ventricular tachycardia (SVT or VT), atrial fibrillation (AF), high-grade and complete AV block, and preexcitation.3,8

Thoracic Radiology

Thoracic radiographs should be obtained as part of the clinical evaluation whenever cardiac disease is suspected. It is, of course, always important to integrate physical examination findings, laboratory determinations (such as arterial blood gas [ABG] analysis), and thoracic imaging studies to arrive at an accurate diagnosis. Practical considerations in adult animals often limit thoracic radiographic imaging to a standing lateral view (Figure 36-2), but this single view is usually adequate to distinguish primary airway or pulmonary parenchymal disease from pulmonary compromise caused by left-sided heart failure (Figure 36-3). Thoracic radiography is also useful for identifying pleural effusion, its severity, and its likely cause. In this regard, it is complementary to thoracic ultrasonography. In neonates, thoracic radiography is particularly useful for distinguishing heart disease from the far more common pulmonary parenchymal diseases associated with immaturity or infection. It is often possible to obtain lateral and dorsoventral radiographs in young crias, and two-view studies are advisable whenever they can be accomplished without causing undue stress to the animal. Chemical restraint should also be considered to optimize the quality of the imaging study when the condition of the animal permits. This often causes less duress compared with physical restraint.

The base of the heart is normally tilted slightly cranially in llamas and alpacas, and the cardiac long axis is normally oriented parallel to the ribs and perpendicular to the thoracic spine. The carina is typically located at the fourth rib or in the fourth intercostal space. The ratio of heart height to the height of the thorax, both measured along the cardiac long access, ranges from 0.68 to 0.74 in healthy adult llamas, and 0.65 to 0.84 in alpaca crias.8,9 Cardiomegaly is usually obvious in camelids with serious heart disease and is typically revealed by an increase in cardiac width beyond three intercostal spaces, an increase in heart height beyond three fourths the height of the thorax, and elevation of the trachea with reduction in the angle of divergence from the thoracic spine below the reported normal range of 10° to 19° (mean 14.4° + 2.0°) in adult llamas, and 9° to 22° (mean 14.2° + 3.6°) in alpaca crias.^8,9 Using a modification of the Buchanan vertebral heart score (VHS) system, Mattoon and colleagues have provided scaled criteria for identifying cardiomegaly in llamas.⁸ According to this method, the height plus width of the normal adult llama heart ranges from 7.7 to 9.1 “vertebral lengths” (mean VHS = 8.4) or 2.75 to 3.55 times the distance from the cranial aspect of T3 to the caudal aspect of T5. In crias, the ratio of cardiac height plus width to T3-T5 has been reported as 3.12 ± 0.21, which is very similar to adult animals. Left heart enlargement is usually easily identified on the lateral radiograph, but reliable identification of right heart enlargement is often more problematic. In young crias, dorsoventral thoracic radiography allows for more sensitive detection of right heart enlargement. In crias, the mean cardiac height plus width to T3-5 ratio on dorsoventral radiography has been reported as 2.5 ± 0.25 and the cardiac to thoracic width ratio as 0.80 ± 0.06. Ambiguous radiographic findings can often be clarified by an echocardiographic evaluation, which is much more accurate for identifying specific patterns of chamber enlargement.

The pulmonary vasculature should be routinely and systematically evaluated on thoracic radiography, and discrepancies in the absolute and relative size of the arteries and veins should be noted. In young crias, the ratio of the right cranial pulmonary artery to third rib has been reported as 0.42 + 0.11 and the ratio of the right cranial pulmonary vein to third rib as 0.45 + 0.11. In adult llamas, the ratio of the right cranial pulmonary artery to the height of T4 is reported as 0.28 ± 0.04 and the ratio of the right pulmonary vein to the height of T4 as 0.30 ± 0.04. Thus, in normal camelids, the cranial lobar pulmonary veins are similar in size or only slightly larger than the accompanying arteries. Developing left heart failure should be considered when the pulmonary veins are substantially larger than the arteries. When interstitial or alveolar perihilar infiltrates are identified together with enlarged pulmonary veins and an enlarged left atrium, congestive heart failure (CHF) is likely. In animals suspect for congenital heart disease, pulmonary overcirculation, resulting from a left-to-right–shunting PDA or VSD, is typically evidenced by concurrent enlargement of the cranial lobar arteries and veins together, with an overall increase in the opacity of the lungs. Right-to-left shunts, in turn, are usually evidenced by diminutive pulmonary vessels and reduced opacity of the lung fields. Evaluation of caudal vena caval size is also easily accomplished on lateral radiography, and this assessment takes on added importance in camelids when right heart failure is suspected, since jugular venous distension cannot be readily evaluated by physical examination. As a general rule, the diameter of the caudal vena cava should not exceed the height of the body of the fourth thoracic vertebrae.

Echocardiography

Echocardiography is essential for the evaluation of all congenital heart diseases and most acquired heart diseases and is particularly well suited for the detection of pericardial effusion. The techniques used to perform echocardiography in camelids do not differ substantially from those used in other large animal species. Low-frequency transducers, ranging from 2 to 3.5 megahertz (MHz), are required to adequately examine adult animals. In crias, either a 5-MHz or a 7.5-MHz transducer provides the necessary resolution required for optimally imaging immature patients. Uncooperative subjects should be sedated if their clinical condition is sufficiently stable. Interrogation of the heart is typically accomplished from a combination of imaging windows located at the ventral aspect of the fourth or fifth intercostal space on the right side of the thorax and at the cardiac apex on the left. To obtain optimal images from the right side, it is very helpful to have the right forelimb positioned as far forward as the animal will accommodate so that the ultrasound transducer can be positioned as far cranial and dorsal as the lung permits. From this location, two-dimensional images should be obtained in six short-axis imaging planes through the left ventricle: (1) through the cardiac apex, (2) at the level of the papillary muscles, (3) the chordae tendineae, (4) the mitral valve, (5) the heart base at the level of the aorta and left atrium, and, if possible, (6) at the level of the main pulmonary artery as it bifurcates at the origin of the left and right pulmonary arteries (Figure 36-4). Two long-axis imaging planes should be recorded from this same location by rotating the transducer counterclockwise to obtain an image plane that optimizes a view of the left ventricular outflow tract and another imaging plane optimizing a view of all four chambers of the heart together with the mitral and tricuspid valves (Figure 36-5). Echocardiography may also be used to examine the heart of the fetus for malformations (Figure 36-6).

With modern echocardiography, M-mode images can be derived (postprocessed) from the digitized two-dimensional images (Figure 36-7). Alternatively, two-dimensional imaging may be used to guide the orientation of the M-mode beam to obtain the desired imaging location. Relevant measures of chamber size may be made from either the two-dimensional or M-mode images permitting the calculation of a variety of functional indices. Normal M-mode echocardiographic measures that are available are based on one study of 23 healthy llamas weighing 110 to 166 kg (mean = 138 kg) and another study of 27 healthy alpacas weighing 43 to 101 kg (mean = 68 kg).^3,10 The reported normal ranges are very wide, reflecting the inclusion of animals with widely differing body weights. M-mode echocardiographic data from a small population of crias (12 alpacas and 5 llamas) were also recently made available.³ Left ventricular (LV) fractional shortening (%FS), calculated as the % change in LV short-axis diameter from end-diastole to end-systole, is the most commonly used index of systolic function. As a rule of thumb, %FS should be 25% or greater in healthy camelids, regardless of age, breed, or sex.

Two-dimensional color flow Doppler imaging is a particularly useful and cost-effective imaging modality for the evaluation of camelids with congenital or acquired heart disease. Not only can the architecture of the heart be easily visualized and accurately measured, but flow disturbances within the heart and great vessels can be easily appreciated and quantified. Images are initially obtained from the right side of the thorax, where flow disturbances in the vicinity of the pulmonic, aortic, mitral, and tricuspid valves can often be appreciated. From this location, accurate flow velocity determinations via spectral Doppler can be achieved only for flow through the pulmonic valve, as such measures require the interrogating ultrasound beam to be parallel with the direction of flow. Nonetheless, it is often possible to document flow disturbances resulting from aortic, mitral, and tricuspid valvular insufficiency or from a VSD via the right parasternal long axis views (Figure 36-8). Echocardiographic imaging from the left apical region on the left side of the chest allows the generation of four-chamber and five-chamber views of the heart, the latter referring to the inclusion of the four cardiac chambers plus the LV outflow tract together with the proximal aorta. This view is particularly useful for evaluating the velocity of blood flow as it moves away from the transducer while flowing out through the aortic valve. Increased flow velocity usually indicates outflow tract obstruction, but mildly increased flow velocities may also be observed with left-to-right shunts and other causes of increased stroke volume. Quantification of valvular stenosis and insufficiency via the modality of spectral Doppler velocity recordings has supplanted cardiac catheterization as the preferred method for determining disease severity. Transvalvular flow velocities recorded in healthy llamas and alpacas are very similar to those reported for dogs and cats. It is noteworthy that often very small jets of valvular insufficiency are present in the immediate vicinity of all the cardiac valves in healthy camelids, and such observations should not be considered indicative of valve disease.¹¹

Arterial Blood Gas Analysis

ABG analysis is useful for determining whether a suspected cardiac abnormality has led to significant right-to-left shunting of blood. Right-to-left shunting allows deoxygenated venous blood to enter the aorta without passing through the lungs, reducing the partial pressure of oxygen (PaO₂) below reference values. Affected animals have a decreased activity level or tolerance for exercise. To differentiate shunting from other causes of hypoxemia, presupplemental and postsupplemental oxygen concentrations may be compared; shunts prevent an increase in PaO₂, whereas oxygenation increases with most other causes of hypoxemia. Serial ABG analyses may be used to track failure, as some animals with left-to-right shunts or a mixture of oxygenated and deoxygenated blood entering the aorta will have a worsening of hypoxemia as left heart failure progresses.

ABG analysis is also a useful diagnostic test in poor-doing animals, particularly neonates and juveniles. Some of these animals will have a covert cardiac defect or acquired valvular disease that does not cause a prominent murmur. Finding hypoxemia, particularly when it does not respond to supplemental oxygen, may be the first clue to direct the diagnostic efforts toward the heart.

Techniques for obtaining arterial samples are described in Chapter 37.

Ventricular Septal Defects

VSDs are far and away the most common congenital anatomic heart defects encountered in camelids.3,10,12,14 VSDs often occur as isolated abnormalities, but they sometimes represent only one component of a more complex cardiac malformation. Accompanying congenital heart defects identified in camelids with a VSD include ASDs, endocardial cushion defects, the various components of ToF, tricuspid valve atresia, TGV, and pulmonary artery hypoplasia. Moreover, VSD may be accompanied by other congenital musculoskeletal, urogenital, and facial abnormalities such as a cleft palate.

The consequences of VSDs depend on size, location, and the presence of other concurrent cardiac malformations. In the majority of affected animals, the VSD is small, and long-term survival without clinical manifestations can be rightly anticipated. Large, isolated VSDs may result in clinical disability either from CHF or as a consequence of pulmonary hypertension. VSDs occur most often in a perimembranous location at the cranial margin of the septal leaflet of the tricuspid valve and just below the supraventricular crest. Less often, VSDs are located immediately below the pulmonic valve in a supracristal, subarterial location. If the aortic annulus is undermined by a VSD positioned high in the interventricular septum, heart failure may develop as a consequence of aortic valve insufficiency resulting from distortion of the right or noncoronary cusps. Not uncommonly, one or more VSDs are identified in the muscular portion of the interventricular septum, where they are referred to as muscular or trabecular VSDs.

In most affected animals, the systolic murmur of a VSD is best heard on the right cranial thorax. Often, an accompanying palpable systolic thrill exists in the same location. The intensity of the murmur is poorly predictive of the size of the lesion, as smaller defects may create greater turbulence through high pressure jets compared with larger defects with more profound hemodynamic consequences. In some affected animals, the point of maximum intensity of the murmur is located at the left heart base, but a right-sided murmur is almost always still identifiable. When the defect is located in the muscular portion of the interventricular septum, the murmur may be heard in a more caudal location on the right side of the thorax near the cardiac apex. On those occasions where aortic insufficiency develops as a consequence of an undermined aortic root, an additional diastolic murmur may be heard in association with the VSD murmur, producing a characteristic “to and fro” type of cardiac murmur. With sufficiently large defects, the volume-overloaded left heart dilates, develops mitral insufficiency, and eventually fails. In animals with very large defects, plexiform lesions develop in the pulmonary arterioles, resulting in the development of irreversible pulmonary hypertension. The resulting reversal of the shunt results in arterial desaturation, exercise intolerance, and central cyanosis. In such cases, no detectable heart murmur may be present.

When the shunt is sufficiently large, thoracic radiography may reveal changes suggestive of a VSD, including evidence of left-sided or biventricular heart enlargement in combination with pulmonary overcirculation, manifested as enlarged pulmonary arteries and veins. However, a definitive diagnosis is usually not possible without resorting to echocardiography (Figure 36-9). Color flow Doppler echocardiography is the preferred method to confirm the diagnosis, allowing visualization of the VSD and estimation of the direction and volume of the resulting shunt. Doppler echocardiography is also particularly useful for detecting pulmonary hypertension or coexisting pulmonic stenosis and for estimating right ventricular and pulmonary artery pressures. VSDs range in size from a few millimeters to the entire expanse of the septum. Most defects are between 0.5 and 1 centimeter (cm) in diameter and located in the membranous portion of the septum in an infracristal location. About one third of VSDs are located above the crista superventricularis. Less often, VSDs are found in the muscular portion of the interventricular septum, particularly near the cardiac apex. It is not uncommon to discover several muscular defects in an affected animal. Given the variability of the location of VSD in camelids, it is important to inspect the entire interventricular septum using a variety of unconventional imaging planes whenever a right-sided murmur is auscultated in a young camelid.

Small VSDs discovered in very young crias may spontaneously close or may never shunt enough blood to cause clinical complications. In general, affected camelids that survive into adulthood without clinical manifestations are unlikely to develop signs later in life. Hence, camelids with small defects do not require treatment. Periodic monitoring by echocardiography is advisable if the integrity of the aortic valve appears threatened or if evidence of significant chamber enlargement exists at the time of initial diagnosis. Common complaints for animals with large VSDs include poor growth, increased time spent in recumbency, and exercise intolerance marked by open-mouthed breathing or recumbency after physical exertion. Treatment of camelids with large VSDs and impending or existent heart failure has largely been limited to the administration of diuretics. Should an owner be particularly intent on optimizing care, a variety of VSD occlusion devices, designed for human use, are available. Once clinical disease is present, progression of the clinical signs usually leads to a decision to euthanize within a few months. The heritability of VSDs has not been established in camelids but conscientious breeders should consider this possibility, even when the VSD is small and not otherwise an important health concern.

Patent Ductus Arteriosus

PDA is not a particularly common congenital heart defect of camelids and has not been identified as an important cause of left heart failure or clinical disability. On occasion, a small PDA is seen as an isolated finding or in association with a persistent right aortic arch, where it contributes to the formation of a constricting vascular ring. More often, a PDA is discovered as part of a more complex defect, where it plays an important role in providing adequate blood flow to the pulmonary circulation when normal perfusion is impaired by right ventricular outflow tract obstruction. In those cases, a continuous (machinery) heart base murmur may be present and accompany other murmurs associated with other cardiac defects.

The exact time of ductus closure in healthy neonatal camelids has not been established with certainty, but it is not unusual to auscultate a soft continuous murmur at the left heart base in crias at 3 or 4 days of age. Color flow Doppler echocardiography often demonstrates a small transductal jet during this period. It is rare to detect such murmurs or to ductal flow by echocardiography after age 1 week.

Atrial Septal Defects and Patent Foramen Ovale

ASDs are far less common causes of clinical disease compared with VSDs, and anecdotal postmortem evidence suggests that they are altogether uncommon in camelids. Several different types of ASD are recognized. Ostium primum ASDs, located in the lower portion of the interatrial septum, may occur as isolated defects or as a manifestation of a complete endocardial cushion defect, sometimes referred to as an atrioventricular septal defect. Ostium secundum ASDs develop in the middle of the interatrial septum, in the region of the fossa ovalis, and are the most common type of ASD. Sinus venosus ASDs occur in the uppermost region of the interatrial septum, typically in association with anomalous pulmonary venous drainage. In crias, the foramen ovale is patent at birth and usually closes within the first 2 weeks of life. In the absence of cardiac enlargement, a patent foramen ovale (PFO) is generally regarded to be of little consequence, as the higher left atrial pressure results in physiologic closure of this potential communication between the atria. Significant shunting across a PFO only becomes problematic when another cardiac disorder causes an increase in atrial pressure and atrial enlargement sufficiently severe to allow shunting similar to that seen with a small secundum type ASD. We have also seen a 12-year-old alpaca with a PFO and bilateral CHF, in which we suspected the defect may have played a contributory role to the severity of its condition.

Interestingly, the soft systolic ejection murmur of a left-to-right shunting ASD resembles the innocent or physiologic murmurs often heard in young crias as well as the soft murmur of mild pulmonic stenosis. Thus, murmurs resulting from ASDs are best heard at the left heart base and rarely exceed grade 3 of 6. Such murmurs are the result of an increased stroke volume passing through the right ventricular outflow tract rather than the quiescent shunting of blood within the atria. Fixed splitting of the second heart sound may sometimes be noted and is a useful clue to the presence of an ASD. Right-to-left shunting through a PFO may be seen in crias with pulmonary and tricuspid stenosis, pulmonary and tricuspid atresia, and other congenital heart defects resulting in elevated right atrial pressure. Small and even moderate-sized ASDs are generally well tolerated. Clinical signs are uncommon unless the defect is quite large or accompanied by other cardiac abnormalities. In the former circumstance, signs of right heart failure may develop during the first few years of life. To date, no treatments beyond supportive care have been reported.

Congenital Valve Stenosis and Insufficiency

Semilunar valve stenosis has been reported in camelids, but such defects are uncommon. We have evaluated several alpacas with moderate isolated pulmonic valve stenosis. More often, lesions of the pulmonary outflow tract comprise one of several anatomic defects such as ToF (see “Cyanosis-Producing Defects” below). Aortic stenosis appears to be particularly uncommon in camelids. Congenital aortic and pulmonic valvular insufficiency are also apparently very rare, as is dysplasia of the mitral or tricuspid valves.¹⁷ Mitral dysplasia causes respiratory compromise and exercise intolerance when severe, whereas tricuspid defects result in jugular distention, jugular pulses, pleural effusions, and ascites. Hematocysts are sometimes observed on the AV valves at necropsy, but such lesions rarely result in valvular insufficiency. Confirmation of a suspected congenital valvular defect is best accomplished by echocardiography. No reports describing the treatment of such defects in camelids have been published.

Cyanosis-Producing Congenital Heart Defects

Complete endocardial cushion defects have been reported in a number of camelids, including a pair of llamas with a common dam.¹⁶ This malformation, sometimes referred to as an AV septal defect or AV canal, consists of lesions involving those structures formed by the endocardial cushions, including the lower portion of the atrial septum and upper portion of the ventricular septum, the septal leaflet of the tricuspid valve, and the anterior leaflet of the mitral valve. The consequence of this combination of lesions is admixture of oxygenated and unoxygenated blood within a “single chamber” compounded by the volume loads resulting from AV valvular insufficiency. A systolic murmur is typically present in such cases and may often be heard on both sides of the chest. Affected camelids usually display clinical signs within the first weeks or months of life. These signs include weakness, cyanosis, lethargy, exercise intolerance, increased time spent in recumbency, decreased nursing, open-mouthed breathing, dyspnea, and poor growth. Engorged jugular and other peripheral veins, pleural effusion, ascites, and passive congestion of the abdominal organs may be present. Echocardiography reveals the communicating heart chambers (Figure 36-10). Color flow Doppler echocardiography reveals dramatic lesions with bilateral AV valve insufficiency and shunting through the combined ASD and VSD. All chambers of the heart are enlarged, but the right side is often enlarged to the extent that it provides the apex of the heart. Severe systolic dysfunction is typically present and pulmonary hypertension may also be evident. Although one llama appears to have survived adequately for 1 year at less than 300 meters (m) above sea level, other affected camelids have shown clinical signs at a young age. Once clinical signs develop, the affected animal usually dies or is euthanized within a few weeks or months. Interestingly, one affected 2-year-old llama began to show signs only after spending a year at high altitude. Diuretics have been used to palliate the clinical signs, but they do not have much effect on the progression of the disease or the eventual outcome. The occurrence of this defect in two related camelids raises the likelihood of a genetic cause, but the heritability of this defect remains speculative.

ToF is another well documented cyanosis-producing cardiac defect occurring in camelids and is characterized by pulmonary stenosis with hypoplasia of the pulmonary arteries, a high VSD, an enlarged and dextropositioned aorta, and right ventricular hypertrophy. This constellation of findings is the result of maldivision of the conotruncal septum during embryonic development. Extreme variants of this abnormality include those cases in which the pulmonic valve and the main pulmonary artery are completely atretic, creating the appearance of a “pseudo” truncus arteriosus (Figure 36-11). In such cases, pulmonary perfusion is accomplished by a PDA connecting the aorta to the right and left pulmonary arteries. Acyanotic forms of ToF are also seen when the pulmonic stenosis lesion is mild and right ventricular systolic pressures are not elevated above the pressure in the left ventricle. Echocardiography is particularly useful for identifying the complex anatomy of all the components of these complex congenital heart defects. Effective treatment requires surgical repair of the observed defects and, to our knowledge, this has not been accomplished in camelids.

TGV has been documented in both llamas and alpacas on multiple occasions, yet this disorder is very uncommon in other domesticated animals. In this condition, the pulmonary artery arises from the left ventricle and the aorta arises from the right ventricle (Figures 36-12 and 36-13). This anatomic arrangement is not compatible with life unless some of the oxygenated blood returning from the lungs is able to pass from the left to the right side of the heart via an intracardiac communication or from the pulmonary artery to the aorta via a PDA. A variety of other cardiac malformations, including abnormalities of the coronary arteries, may also be identified. Affected individuals are always severely cyanotic at birth, and they usually survive only a short period. Other complex cyanosis-producing cardiac abnormalities, including hypoplasia of the left ventricle and double outlet right ventricle, have been seen in New World camelids (Figure 36-14).

Vascular Ring Anomalies

Vascular ring anomalies have been reported in both alpacas and llamas.18,19 In contrast to other domestic species, the most common abnormality identified is a left aortic arch with either a right ligamentum arteriosum or small right PDA. This anomaly is often accompanied by aberrant origination of the right subclavian artery (Figure 36-15). The more familiar right aortic arch with constricting left ligamentum has also been observed. In those cases with a PDA, the size of the shunt was small, and a continuous murmur was only noted in one affected alpaca. Most affected animals presented at ages 3 to 5 months, and the clinical signs were largely attributable to constriction of the esophagus. Dysphagia, abnormal regurgitation, choke, bloat, and failure to thrive are common clinical signs. Cough may also occur as a consequence of tracheobronchitis or pneumonia caused by inoculation of the airways with swallowed and regurgitated food. On occasion, the development of clinical signs may be delayed until early adulthood. Routine thoracic radiography often demonstrates a dilated esophagus both cranial and caudal to the heart base, sometimes with retained ingesta. It is sometimes possible to identify a persistent right aortic arch on a dorsoventral thoracic radiograph, but other vascular ring malformations may easily escape detection.

Esophagoscopy, contrast esophagography, or fluoroscopy may be performed to confirm the stenotic lesion in the esophagus at the heart base (see Figure 36-15), but visualization of the vascular malformation responsible for the constriction is best accomplished by using angiography or contrast-enhanced computed tomography (CT). Inasmuch as the surgical approach to attempt repair is dependent on the precise nature of the malformation, consideration should be given to sophisticated imaging studies whenever surgical repair is contemplated. Surgical repair has been attempted, but success has been limited, partially because of concurrent aspiration pneumonia.

Other Vascular Defects

A portosystemic shunt has been reported in one juvenile alpaca with diarrhea, poor growth, and excessive tractability for its age.²⁰ Serum bile acid and blood ammonia concentrations were very high, and serum hepatic enzyme activities were within reference values, supportive of a diagnosis of vascular shunt. A colonic mesenteric vein portogram revealed a large extrahepatic shunt to the caudal vena cava, which was surgically ligated. The cria appeared to recover physically, behaviorally, and biochemically.

Two unrelated adult alpacas were reported to have networks of large, tortuous, anastomosing vessels in the right cranial lung lobe.²¹ On the basis of the predominance of tunica media over tunica adventitia, the abnormal vessels were judged to be arterial in origin. The older alpaca had severe bilateral epistaxis and pulmonary hemorrhage linked to rupture of one of these vessels. In the younger alpaca, the vascular anomaly was considered an incidental finding, with speculation that it might have become problematic with time. In humans, such lesions are often considered congenital and usually contain arteriovenous shunts.²² Approximately one quarter of the cases progress with time, whereas the majority remain static. Imaging studies were not performed on the alpacas but might have revealed the unusual vascularity. Vessel ligation or embolization or en bloc resection (lobectomy) have been used to treat this condition in other species.

Pericardial Disease

Pericardial disease is uncommon in llama and alpacas, and only a few reports of pericardial disease appear in the literature.3,23–25 Echocardiographic identification of pericardial effusion is the most common diagnostic test (Figure 36-16). One case of pericardial effusion causing cardiac tamponade has been reported in a 2-year-old pregnant alpaca.²³ In this case, successful treatment was accomplished by pericardiocentesis and administration of antibiotics and antiinflammatory drugs. Bacteria were not cultured from the pericardial fluid in this case, and the cause of the effusion is best regarded as idiopathic. Constrictive effusive pericarditis has also been reported in a single case report of a successfully treated llama cria.²⁴ In another successfully treated cria, pericardial effusion led to electrical alternans on ECG.²⁵ An unrecognized septic event was thought to be the inciting factor. Others have identified pericardial effusion in association with a variety of disorders, including dilated cardiomyopathy, pleuropneumonia, pulmonary hypertension, and several different types of congenital heart disease. We have observed small effusions in a few llamas and alpacas with severe heart failure, which we considered an incidental secondary finding and of no great clinical significance. Mild effusion may occur with hypoproteinemia as well.

To obtain a diagnostic sample or to relieve pressure on the heart, ultrasonography-guided pericardiocentesis may be performed through the fourth intercostal space on either side, taking care to avoid hitting the heart.

Endocarditis

Endocarditis is an important but, fortunately, infrequent disorder of camelids.26–28 In most domestic animal species, endocarditis lesions are mainly confined to the cardiac valves and mural lesions are uncommon. In camelids, mural lesions within the ventricles have been observed more often and are more dramatic than valvular lesions, at least in the population of animals evaluated at Oregon State University (Figure 36-17). In our experience, the endocardial surface of the right ventricle is more commonly affected than the left, although both ventricles are affected in half the cases. Often, the leaflets of the AV valves become embedded within the thrombotic material, with the tricuspid valve slightly more commonly affected than the mitral valve. It is usually difficult to identify a remote source of infection as the primary cause of endocarditis, although preexisting abnormalities have been identified in several reports. Bacterial organisms may sometimes be recovered either via blood culture or at necropsy, but it is often not possible to recover microorganisms before or after death.

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