Chapter 151 Pericardial Diseases
The pericardium consists of two mesothelial-lined membranes: the visceral layer (epicardium) that is tightly adhered to the myocardium and the reflection of this membrane that forms the parietal pericardium. Between these is a space that contains the heart, origins of the major arteries, and terminations of the vena cava and pulmonary veins. The normal pericardial space also contains a very small amount of serous, lubricating pericardial fluid. The normal pericardium limits acute cardiac dilatation, maintains cardiac geometry, contributes to ventricular compliance and interdependence, reduces friction, and provides a barrier from inflammation. The pericardium is not essential to survival and can be removed surgically.
• The most important congenital forms of pericardial disease are congenital peritoneopericardial diaphragmatic hernia (PPDH) and the relatively rare congenital pericardial cysts (which will not be discussed in this chapter).
• The main acquired pericardial diseases in dogs and cats are pericardial effusion (PE), constrictive pericarditis, and constrictive-effusive pericardial disease. In many cases, PE is related to the presence of a cardiac or heart-base neoplasm.
• Cardiac tamponade refers to a state of cardiac compression and impaired filling from increased intra-pericardial pressure. While mass lesions and cysts can compress the heart, the majority of cases are caused by a PE.
• The total volume within the pericardial space is finite. Pericardial fluid accumulation can occur only if the parietal pericardium stretches (increasing the volume of the pericardial space) or the volume within the cardiac chamber shrinks.
• Since the parietal pericardium contains few elastic fibers, it is not easily distended in the setting of acute fluid accumulation. For this reason, even small volumes of acute intra-pericardial hemorrhage can produce cardiac tamponade.
• When parietal effusion develops more gradually, the parietal pericardium and pericardial space expand substantially. Progressive pericardial stretching, combined with increases in venous pressure, permit a situation in which large volumes of PE may develop. Effusions exceeding one liter may accumulate in larger dogs.
• Pericardial constriction occurs secondary to pericardial inflammation or scarring. The normally strong pericardium becomes thicker and fluid within the space is reabsorbed. Eventually the pericardial membranes act as a “shrink wrap” about the heart.
• Constrictive-effusive pericardial disease is a condition that includes both pericardial restriction and a small volume of pericardial fluid.
PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA
Diagnosis
Physical Examination
• The diagnosis may first be suspected during routine examination as heart sounds may be muffled or displaced.
• Often there is a systolic murmur, which may be functional or represent a concurrent cardiac defect.
Diagnostic Imaging
• One typically observes altered radiographic density in the caudoventral portion of the pericardial space. The heart and carina are usually displaced craniodorsally, as are pulmonary venous entries to the left atrium.
• Ventral to the caudal vena cava there may be a soft tissue shadow, the persistent mesothelial remnant that delineates the dorsal border of the hernia.
• Ultrasonography of the thorax, or a barium swallow (if intestinal loops are present) will be diagnostic.
PERICARDIAL EFFUSION
Etiology
• Transudation into the pericardial space occurs secondary to PPDH, right-sided CHF, cysts, hypoalbuminemia, infections/toxemia, and causes of increased vascular permeability. These fluid accumulations tend to be relatively small and are often incidental necropsy or ultrasound findings. Small effusions do not to impair heart function. There are two noteworthy clinical situations that do merit comment.
• Mass lesions at the heart base, including chemodectomas, can obstruct lymphatic drainage leading to a large and compressive transudative PE.
• Exudation into the pericardial space is usually caused by infective or non-infective pericarditis; these conditions are relatively uncommon in small animals.
• Nocardia infection and perforating foreign bodies are potential causes of septic pericarditis in dogs and cats.
• Fungal involvement of the pericardium is recognized with coccidiomyocosis in the dog or with opportunistic fungi in immunosuppressed dogs (e.g., aspergillosis).
• Idiopathic, sterile (inflammatory) pericarditis can develop occasionally in the dog and also may be a consequence of recurrent, idiopathic intrapericardial hemorrhage.
• Idiopathic intrapericardial hemorrhage (with or without secondary pericardial reaction) is relatively common in dogs. This is a disorder of dogs typically less than 7 or 8 years of age, though it can occur in older dogs. As the name suggests, the etiology is unknown. Recurrent bleeding evokes an inflammatory reaction with pericardial thickening that can be difficult to distinguish from mesothelioma. Constrictive or constrictive-effusive pericardial disease can develop.
• Neoplasia of the heart, heart base, or pericardium frequently leads to a hemorrhagic effusion in dogs.
• Hemangiosarcoma of the right atrium is especially common in dogs >7 years of age. Tumors can be isolated to the heart or multicentric with splenic involvement and pulmonary or distant metastasis. Metastatic disease is very common.
• Aortic body tumor (or chemodectoma) originates from the base of the aorta and grows along the heart base, often along the path of least resistance. Metastatic disease is very unusual.
• Ectopic (heart-base) thyroid carcinoma can cause a large heart base mass that is more likely to invade the myocardium.
• Mesothelioma of the pericardium also occurs frequently, but the diagnosis is often difficult as discussed below. Progressive growth is typical and the pericardium may scar or constrict.
• Lymphosarcoma of the right atrium and ventricles is an important cardiac neoplasm in the cat but is considered a rare cause of PE in dogs. It is frequently multicentric.
• Left atrial rupture can occur in dogs with mitral regurgitation from chronic valvular endocardiosis. Linear tears develop within the stretched left atrial wall and occasionally transmural separation occurs leading to sudden cardiac tamponade.
• Uncommon causes of pericardial hemorrhage include blunt chest trauma; puncture of the heart (knife, bullet, and missile); coagulopathy, and as a complication of thoracocentesis.
Pathophysiology
• The cause and underlying pathophysiology of a pericardial disorder influences the clinical presentation. An understanding of these processes (Fig. 151-2) is instructive relative to diagnostic studies and therapy.
• Inflammatory disease within the pericardial space may create clinical signs related to localized chest discomfort or constitutional signs of systemic inflammation. This is especially true in cases of septic pericarditis.
• Cardiac tamponade is the major pathophysiologic event in PE and represents the state of cardiac compression caused by increased intrapericardial fluid pressure. The normally negative inspiratory pericardial pressure becomes positive. This can be documented in clinical cases by a simple fluid manometer attached to a drainage catheter that has entered the pericardial space.
• Tamponade is the mechanism by which low cardiac output and congestive heart failure (CHF) develop with PE.
• Intrapericardial pressures can rise rapidly as the elastic limits of the membrane are exceeded (a steep pressure to volume relationship).
• Increased (positive) intrapericardial pressure develops leading to diastolic collapse of the right atrium and the right ventricle along with compression of the vena cava.
• Reduced right ventricular filling decreases preload and cardiac output; systemic hypotension occurs if sympathetic and fluid-retaining compensatory mechanisms are insufficient.
• However, given sufficient time ABP is reestablished by combinations of heightened sympathetic discharge, systemic vasoconstriction, renal retention of sodium and water, and elevated venous pressures.
• Extremely high venous pressures are characteristic of chronic pericardial diseases. Congestive heart failure, with a predominately right-sided component (ascites, pleural effusion, subcutaneous edema) is the consequence of chronic cardiac tamponade or constriction.
• Pulsus paradoxicus is readily identified by palpation or ABP measurement with a Doppler flow system and is defined as an exaggerated fall in the ABP and pulse pressure during inspiration (see “Physical Examination”).
• Pulsus paradoxicus is explained by exaggeration of the normal respiratory-induced variation in right and left-sided cardiac filling. Left ventricular filling and systemic arterial pressure fall as right ventricular filling is augmented by negative inspiratory pleural pressures. Since the total volume with the pericardial space is finite, the increased venous return shifts the ventricular septum into the left ventricle during inspiration, reducing LV preload and stroke volume. As a result, palpable pulse pressure and measured systolic ABP decline during inspiration and increase with expiration as the process is reversed.
Diagnosis
Physical Examination
• Patients with acute cardiac tamponade may be hypotensive with palpable distention of the jugular vein. A systolic ABP <90 mm Hg should be treated as an emergency with consideration for prompt pericardiocentesis.
• Elevated jugular venous pressure, distant heart sounds, and respiratory variation in blood pressure (pulsus paradoxicus) constitute the classic “triad” of physical findings in cardiac tamponade.
• The central venous pressure is generally quite high in PE, often exceeding 12 cm H2O [normal <5 cm H2O].
• The recognition of pulsus paradoxicus is not difficult and, in some cases, is obvious from simple palpation of the femoral arteries.
• When using a Doppler flow method for diagnosis, the pressure cuff should be slowly deflated to identify a consistent inspiratory fall and expiratory rise in systolic blood pressure. The intensity of the Doppler flow sound also changes, becoming fainter during inspiration (indicated reduced stroke volume).
• Pulsus paradoxicus is highly suggestive, though not specific for cardiac tamponade. Respiratory distress with marked variation in intrathoracic pressure can also lead to respiratory variation in the pulse. Panting can make it difficult to recognize pulsus paradoxicus.
• Right-sided CHF is more typical of PE and is associated with elevated jugular venous pressure, hepatomegaly, ascites, and possibly pleural effusion. In one study, CHF was more commonly associated with idiopathic pericardial hemorrhage. Experimental PE in dogs leads to interstitial lung edema, but in clinical cases, it is rare to diagnosis overt left-sided CHF.
• Cardiac auscultation of PE is characterized by muffled heart sounds. A pericardial friction rub may indicate pericarditis, but this is atypical of dogs and cats with PE.
• Breath sounds are muffled and there will be tachypnea or respiratory distress when pleural effusion complicates pericardial disease.
Laboratory Tests
• Routine blood tests in pericardial disease may simply reflect the consequences of heart failure or prior diuretic therapy.
• The CBC may indicate inflammation, infection, or hemorrhage. Increased numbers of circulating nucleated RBCs are suggestive of hemangiosarcoma of the spleen (and heart). In cases of severe hemopericardium, the patients may be anemic due to blood loss or exhibit the nonregenerative anemia of chronic illness. Evidence of disseminated intravascular coagulopathy is evident with disseminated hemangiosarcoma.
• Serum troponins (cTnI) may increase with PE and are higher in the setting of cardiac neoplasia, especially in cases of hemangiosarcoma.
• Analysis of pleural or peritoneal effusions generally indicates fluid of an obstructive origin (transudate, modified transudate, or infrequently chyle). Bacterial cultures of the effusate, serum fungal titer (coccidiomycosis), or ELISA tests for FeLV or FIP (cats) may be positive when pericarditis is related to these infections.
Electrocardiogram
An electrocardiogram may show any of the following:
• Decreased amplitude QRS complexes (<1 mV in all frontal plane leads in dogs). This finding is common but inconsistent.
• Electrical alternans (with large effusates and swinging of the heart). This is a relatively specific but insensitive finding in PE.
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