CLINICAL SIGNS

The rapidity of onset of clinical signs of pericarditis varies considerably, ranging from acute pericardial fluid accumulation to slower, more chronic fluid accumulation, with or without pericardial fibrosis. Clinical signs are seen when diastolic cardiac filling is impaired, leading to systemic venous congestion and decreased cardiac output. This can develop as intrapericardial pressure increases with pericardial fluid accumulation (cardiac tamponade) or when fibrosis of the pericardium restricts normal distensibility. Development of increased pericardial pressure depends on the volume of pericardial fluid, rate of accumulation, and properties of the pericardium itself. Because the right side of the heart can withstand less transmural pressure than the left side before collapsing, signs of right-sided cardiac dysfunction develop first.

Common owner complaints at initial evaluation are often nonspecific and include fever, poor appetite, lethargy, weight loss, colic, and tachypnea. Signs of cardiac or respiratory tract disease are common reasons for referral of an affected horse from another veterinarian. Clinical signs appreciated in most horses with cardiac tamponade include tachycardia, jugular and other systemic venous distension, ventral edema, weak pulses, pale or cyanotic mucous membranes, and quiet heart sounds if the volume of pericardial fluid is substantial. Clinical signs detected inmany horses with cardiac tamponade include pericardial friction rubs if the effusion is fibrinous, depression, fever, tachypnea or dyspnea, and quiet lung sounds ventrally. Pericardial friction rubs are classically triphasic in that they are heard during atrial contraction, ventricular contraction, and after early diastolic filling.

Pulsus paradoxus may also be detected in horses with cardiac tamponade and is appreciated as an exaggeration of the normal decrease in systemic blood pressure that occurs during inspiration. This decrease is a result of decreased left ventricular stroke volume during inspiration because of increased venous return and right ventricular filling at the expense of left ventricular filling, a transient reduction in the filling gradient between the pulmonary veins and the left atrium, and a decrease in the contribution of the interventricular septum to left ventricular contraction. In my experience, peripheral pulses are sometimes too weak for pulsus paradoxus to be appreciated in horses with cardiac tamponade.

DIAGNOSIS

A hemogram may reveal changes consistent with an infection or a stress leukogram, including leukocytosis, neutrophilia (with or without a left shift), and hyperfibrinogenemia. Results of a serum biochemistry panel may be normal or may indicate dehydration, hypoproteinemia, electrolyte derangements from pericardial accumulation of fluid (third-space fluid), or changes consistent with end-organ damage from cardiac tamponade, such as azotemia and high liver enzyme activities.

An electrocardiogram will likely reveal tachycardia and low-amplitude QRS complexes (Figure 44-1). Electrical alternans, or beat-to-beat alternation of R-wave amplitude, is a specific but not sensitive indication of cardiac tamponade. Radiography may reveal an enlarged cardiac silhouette, but cardiac margins may be difficult to assess if pleural effusion is present.

Stay updated, free articles. Join our Telegram channel

Join