INTRODUCTION

Normally, a small volume (≈0.25 ml/kg) of serous fluid lies between the outer fibrous (parietal) pericardial layer and the serous visceral pericardium or epicardium.¹ Excess, abnormal fluid within this space (pericardial effusion) is a common disorder that has a variety of causes (see Chapter 44, Pericardial Diseases). Pericardial effusion impairs cardiac function when intrapericardial pressure rises and prevents normal cardiac filling. Most pericardial effusions in dogs are serosanguineous or sanguineous; these are usually of neoplastic or idiopathic origin.^2,3 Pericardial transudates, modified transudates, and exudates occasionally occur in both dogs and cats.

PATHOPHYSIOLOGY OF CARDIAC TAMPONADE

The hemodynamic consequences of pericardial effusion depend on the intrapericardial pressure-volume relationship. Because the fibrous pericardium is relatively noncompliant, increases in fluid volume can sharply raise intrapericardial pressure. Cardiac tamponade develops when intrapericardial pressure rises toward and exceeds normal cardiac diastolic pressures.^2-4 The external cardiac compression progressively limits right ventricular filling and, with increasing severity, also reduces left ventricular filling.^2,3,5 Systemic venous pressure increases and forward cardiac output falls. Eventually, diastolic pressures in all cardiac chambers and great veins equilibrate.^2,3

The rate of pericardial fluid accumulation and the distensibility of the pericardial sac determine whether and how quickly cardiac tamponade develops. Rapid accumulation of a relatively small-volume effusion (e.g., 50 to 100 ml) can raise intrapericardial pressure markedly, because pericardial tissue stretches slowly. Conversely, a slow rate of fluid accumulation may allow for enough pericardial enlargement to maintain low intrapericardial pressure until the effusion is quite large. A large volume of pericardial fluid implies a gradual process. So long as intrapericardial pressure is low, cardiac filling and output remain relatively normal and clinical signs are absent. Fibrosis and thickening further limit the compliance of pericardial tissue, and this can increase the likelihood of pericardial tamponade. Pericardial fibrosis and inflammatory cell infiltrates are described with idiopathic as well as neoplastic causes of effusion.^6,7

Neurohormonal compensatory mechanisms are activated as cardiac output falls.^8,9 These contribute to fluid retention and other clinical manifestations of tamponade. Signs of systemic venous congestion become especially prominent over time. Although pericardial effusion does not directly affect myocardial contractility, reduced coronary perfusion during tamponade can impair both systolic and diastolic function. Low cardiac output, arterial hypotension, and poor perfusion of other organs besides the heart can ultimately precipitate cardiogenic shock and death.

Cardiac tamponade also causes an exaggerated respiratory variation in arterial blood pressure known as pulsus paradoxus. Inspiration normally lowers intrapericardial and right atrial pressures slightly, which enhances right heart filling and pulmonary blood flow. Left heart filling diminishes as more blood is held in the lungs and the inspiratory increase in right ventricular filling pushes the interventricular septum leftward. Thus left heart output and systemic arterial pressure normally decrease slightly during inspiration. Patients with pulsus paradoxus exhibit a fall in arterial pressure during inspiration of 10 mm Hg or more.^10,11

CLINICAL PRESENTATION

Cardiac tamponade is relatively common in dogs, but rare in cats. Clinical findings reflect poor cardiac output and usually systemic venous congestion as well. The typical history includes exercise intolerance, abdominal enlargement, tachypnea, weakness, collapse or syncope, and sometimes cough. Collapse is more common in dogs with cardiac neoplasia than in those with idiopathic disease.¹² Nonspecific signs such as lethargy, inappetence, or other gastrointestinal maladies can develop before obvious ascites does.

Physical Findings

Jugular venous distention or a positive hepatojugular reflux,* hepatomegaly, ascites, labored respiration, and weakened femoral pulses are common physical findings.^3,12-15 Pulsus paradoxus is detected occasionally by femoral pulse palpation. High sympathetic tone commonly produces sinus tachycardia, pale mucous membranes, and prolonged capillary refill time. The precordial impulse is palpably weak with a large pericardial fluid volume, and heart sounds are muffled by moderate to large pericardial effusions.^2,12,13 In addition, lung sounds can be muffled ventrally with pleural effusion. Pericardial effusion alone does not cause a murmur, but concurrent cardiac disease may do so. Reduced lean body mass (cachexia) is apparent in some chronic cases.

Although right-sided congestion predominates, signs of biventricular failure can occur. Rapid pericardial fluid accumulation can cause acute tamponade, shock, and death without signs of pleural effusion, ascites, or radiographic cardiomegaly. Pulmonary edema, jugular venous distention, and hypotension may be evident in such cases.