Pericardial Disease

The pericardium limits cardiac dilation, acts as a barrier against contiguous infection, and
contributes to the diastolic properties of the heart. The pericardial space is formed by the
reflection of the two major pericardial membranes, the parietal pericardium and the visceral
pericardium (epicardium), and normally contains such a small amount of serous fluid that it
cannot be seen by echocardiography. Pericardial effusion leading to cardiac compression
(tamponade) impairs ventricular filling and diastolic function, typically causing right-sided
congestive heart failure (CHF).
Some cases of pericarditis progress to constrictive pericardial disease, which severely limits
ventricular filling. Pericardial effusion can develop as a primary disorder or secondary to
pleuropneumonia. Infective pericarditis can produce an effusion sufficient to cause cardiac
tamponade or eventual constriction of the heart.
Sterile, idiopathic pericardial effusion also has been reported in horses. The volume of effusion
can be substantial and can lead to cardiac decompensation. Cardiac mass lesions and
intrapericardial tumors have been reported sporadically. Cranial mediastinal tumors
(lymphosarcoma) or abscesses secondary to pleuropneumonia also can compress the heart and
mimic pericardial disease.
Myocardial Disease
The myocardium forms the bulk of the atrial and ventricular muscular walls. The right
atrium (RA) communicates with the RV inlet through the right atrioventricular (AV) or tricuspid
valve. The RV appears crescent shaped on cross-sectional echocardiographic examination and is
functionally U shaped. The RV inlet is located in the right hemithorax and the outlet, pulmonary
valve, and main pulmonary artery (PA) on the left side of the chest. The left atrium (LA) is
caudal to the RA and separated by the atrial septum. The LA is dorsal to the LV through which it
communicates across the left AV (mitral) valve. The LV is circular in cross section when viewed
by echocardiography and separated from the RV by the ventricular septum. The septum and
free walls are thicker than the RV free wall (by approximately 2.5–3 times).
Persistent embryologic openings in the cardiac septa are known as septal defects, with
the ventricular septal defect (VSD) representing the most common cardiac anomaly in most
equine practices. The LV is functionally V shaped, with an inlet and outlet separated by the
cranioventral (septal or according to the human nomenclature “anterior”) leaflet of the mitral
valve. The aorta originates in the LV outlet, continuous with the ventricular septum cranially
and in fibrous continuity with the septal mitral leaflet caudally. This great vessel exits from near
the center of the heart and to the right of the main PA. The myocardium may dilate or
hypertrophy in response to exercise, in response to increased work caused by