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Cardiovascular System

Normal structure

The bird's heart sits squarely in the middle of the coelomic cavity just caudal to the thoracic inlet. The axis of a normal heart deviates only slightly from the midline. Enlargement of any of the chambers may result in a change in the heart axis. The cranial ventral surface of the heart is in contact with the sternum, and the liver lobes cover the apex of the ventral surface.

The thin-walled atria have a scalloped surface and margins and are symmetrically located at the base of the heart. The right atrium is somewhat larger than the left. The right atrioventricular (AV) valve is a single muscular flap and is not membranous. The right ventricular free wall wraps around the heart from the caudal right lateral aspect of the heart to the cranial ventral surface of the heart. The wall of the right ventricle is approximately one-third to one-half the thickness of the interventricular septum and the free wall of the ventricle. This ratio, however, varies to some degree with the species, between individuals within species, and also varies depending on what level of the heart the measurements are taken.

The pulmonary and aortic values are essentially the same as those found in mammals. The left AV valve is membranous but is a continuous sheet and does not have clearly defined cusps. The valve is connected to papillary muscles by chordae tendineae. The brachiocephalic trunks immediately branch off the aorta as it leaves the heart. The first arteries to leave the brachiocephalic trunks are the carotids, which are relatively thin walled and narrow. The aorta arches to the right in the bird, as opposed to the left in mammals. Birds have a larger heart compared with body mass than do mammals. Myocytes have a smaller diameter (approximately one-fifth to one-tenth) than those found in mammalian hearts and a more rapid depolarization leading to a faster heart rate and relatively greater cardiac output. Purkinje fibers of the conduction system are relatively large as compared to those found in mammals.

Congenital anomalies

Most of the literature on avian heart anomalies concern chickens. Congenital lesions in pet birds are rarely described. Ventricular septal defects appear to be relatively common in umbrella cockatoos, and one of the authors (D.N.P.) has also seen them in cockatiels and an African grey parrot. The defects between the ventricles are typically 1-3 mm in diameter and are located in the interventricular septum just below the pulmonary and aortic valves (Fig. 1.1). Right- and left-sided heart failure typically develops in these birds between 1 and 3 years of age. Dilation of both ventricles is common, and the pulmonary veins are markedly distended (Fig. 1.2). Perihepatic effusion and cirrhosis of the liver with dilation of the hepatic veins may be present secondary to right-heart failure. Interventricular septal defects have also been associated with a truncus ateriosis in an umbrella cockatoo and aortic hypoplasia in a Moluccan cockatoo (Cacatua moluccensis).

Figure 1.1 Interventricular septal defect (arrowhead).

Figure 1.2 Marked distension of pulmonary veins (arrows) secondary to right-sided and left-sided failure in a bird with an interventricular septal defect.

Congenital aneurysms of the left ventricle are uncommon. One of us (D.N.P.) has seen several of these in cockatiels. All were small, typically 2-4 mm in diameter. A large left ventricular aneurysm (2 cm in diameter) was found in a mature blue and gold macaw. All of these emanate from the apex of the heart. There was no other evidence of heart disease in these birds and the lesion was not thought to impact the heart function.

An epicardial keratinaceous cyst presented as a yellow nodule containing caseous material. Histologically it was lined by stratified squamous epithelium, and the grossly noted material was laminated keratin. Based on the gross appearance, the differential diagnosis for this type of lesion would be an abscess. We have seen an African grey parrot with a focus of capillary proliferation in the myocardium (Fig. 1.3) that was considered to be congenital telangiectasis or possibly an example of a hamartoma.

Figure 1.3 Congenital myocardial lesion comprised of irregular, dilated vascular channels.

In chickens, cardiac anomalies are thought to be associated with stress during organogenesis, including increased temperature and hypoxia. Vitamin deficiencies may also be responsible for these malformations in chickens. Aortic anomalies are reported in chickens and have been associated with excessively high or low humidity during incubation. Given that ventricular septal defects are seen most frequently in umbrella cockatoos, a genetic defect may be to blame for this anomaly in this species.

Pericardial disease

Pericardial lesions can be a manifestation of infectious, noninfectious, or neoplastic diseases.

Infectious disease

Infectious disease of the pericardium can be localized to the pericardium or may be just one manifestation of a systemic disease. A variety of organisms have been found to cause pericarditis, including numerous bacteria, including members of the Enterobacteriaceae, Mycobacteria, and Chlamydia psittaci, fungi and, occasionally, avian polyomavirus.

Pericarditis causes the pericardium to be variably thickened and gray to yellow-white, with red foci seen occasionally. The pericardium may have a shaggy appearance. In less severe cases, multifocal plaques are seen. There may be adhesions to the epicardium (Fig. 1.4). Pericardial fluid is increased, gray-yellow, and cloudy and may be flocculent. Histologically, bacterial and fungal infections cause edema, fibrin deposition, and an initial purulent response containing numerous heterophils and macrophages. Relatively more lymphocytes and plasma cells may be found in fungal infections. The pericardium may be adhered to the epicardium (Fig. 1.5).

Figure 1.4 Epicarditis and pericarditis due to a systemic infection by Chlamydia. Grossly differential diagnoses include a variety of bacterial infections.

Figure 1.5 Chronic pericarditis/epicarditis. Note the diffuse inflammatory reaction and adherence of the pericardial tissue to the epicardium.

With chronicity, there can be abscess formation. Macrophages and possibly giant cells as well as a more pleocellular response surround a central necrotic area. In both acute and chronic conditions, specificity depends on finding organisms that may be present.

Mycobacterial infections usually present grossly as large irregular masses that can mimic neoplasia. They are relatively firm, gray-white, and most often near the heart base. Early mycobacterial infections elicit a response of heterophils and macrophages. Organisms may be present infrequently. In advanced mycobacterial disease, the response will be primarily large macrophages with abundant light basophilic cytoplasm. Organisms can be seen within the cytoplasm with acid-fast stains.

Noninfectious disease

The pericardium is a common site of visceral urate deposition (gout). Grossly the lesion can be similar to an infectious pericarditis, with a thickened membrane containing gray-white plaques. However, pericardial thickenings associated with gout are typically white, smooth, and shiny as opposed to the yellowish, roughened, and dull exudates seen in infectious conditions. Flocculent material, along with an excess of turbid fluid, may be present in the pericardial sac (Fig. 1.6).

Figure 1.6 Severe pericardial and epicardial urate deposition. The lesion must be differentiated from infection.

Histologically, urates may be crystalline or amorphous and are lightly basophilic on hematoxylin-eosin stains. Although the crystals dissolve in formalin, the remaining characteristic needle-shaped spaces can be found in most cases. Alcohol fixation and special staining can be used if there is any doubt that the lesion is gout. Depending on the duration of the urate deposition, there will be an inflammatory response comprised primarily of heterophils. Focal necrosis may also be seen.

Neoplastic disease

In mammals, sarcomas and mesothelioma have been reported in the pericardium. Primary pericardial tumors are not documented in pet birds, and we have not seen any examples of them.

Pericardial effusion

Effusion may accompany primary heart and pericardial diseases, as already discussed, and may be a part of systemic problems, including anything leading to right-sided heart failure or hypoproteinemia. Effusions may be transudates, modified transudates, exudates, or hemorrhage. The gross appearance will depend on the composition of the fluid. Within several hours of death, high-protein effusions will often become gel-like. In some instances the amount of pericardial fluid may be massive (Fig. 1.7).

Figure 1.7 A large amount of partially coagulated proteinaceous fluid in the pericardial sac leading to cardiac tamponade. The fluid accumulation can be due to a number of causes.

Heart disease

Diseases of the heart can be divided into traumatic inflammatory,...