Pericardial Disease

7 Pericardial Disease



Wendy A. Ware



1. What is the normal structure and function of the pericardium?

The pericardium is a double-layered sac that encases the heart and is attached to the great vessels at the heart base. It consists of an outer fibrous layer (parietal pericardium) and an inner serous membrane covering the heart (visceral pericardium or epicardium). A small amount of clear, serous fluid is normally present between these layers and acts to reduce friction. The pericardium limits acute distention of the heart and maintains normal cardiac position, geometry, and ventricular compliance. The pericardium also forms a barrier to inflammation or infection of surrounding structures.


2. What congenital pericardial malformations are of clinical concern?

Pericardioperitoneal diaphragmatic hernia (PPDH) is the most common pericardial malformation in dogs. Abnormal embryonic development (probably of the septum transversum) allows persistent communication between the pericardial and peritoneal cavities at the ventral midline. The pleural space is not involved. Other congenital defects such as umbilical hernia, sternal malformations, and cardiac anomalies may also be present. Males appear to be affected more frequently than females. Clinical signs are variable and result from herniation of abdominal contents into the pericardial space. Pericardial cysts are rare anomalies thought to originate from abnormal fetal mesenchymal tissue or from incarcerated omental or falciform fat from a small PPDH. Other congenital defects of the pericardium itself are extremely rare in dogs; most are discovered incidentally on postmortem examination. Both partial (usually on the left side) and complete absence of the pericardium have been reported.


3. How is PPDH diagnosed?

Clinical signs associated with PPDH usually develop within the first year or so of life but can appear at any age (cases have been diagnosed between 4 weeks and 15 years of age). Some animals never have clinical signs and are diagnosed fortuitously. Clinical signs are usually gastrointestinal or respiratory. Vomiting, diarrhea, anorexia, weight loss, abdominal pain, cough, dyspnea, and wheezing are most often reported; shock and collapse can also occur. The physical examination may indicate muffled heart sounds on one or both sides of the chest, displacement or attenuation of the apical precordial impulse, an “empty” feel on abdominal palpation (with herniation of many organs), and, rarely, signs of cardiac tamponade.


Thoracic radiography is often diagnostic or highly suggestive of PPDH. Characteristic findings include enlargement of the cardiac silhouette with dorsal tracheal displacement, overlap of the diaphragmic and caudal heart borders, and abnormal fat or gas densities within the cardiac silhouette. On lateral view, a pleural fold is usually evident extending between the caudal heart shadow and the diaphragm ventral to the caudal vena cava. Gas-filled loops of bowel crossing the diaphragm into the pericardial sac, a small liver, or few organs within the abdominal cavity may also be observed. Echocardiography is useful in confirming the diagnosis in animals in which the diagnosis is equivocal. A gastrointestinal barium series is diagnostic if stomach or intestines are in the pericardial cavity. Fluoroscopy, nonselective angiography (especially if only falciform fat or liver has herniated), celiography, or pneumopericardiography also have been used in diagnosis. Electrocardiographic changes are inconsistent; decreased amplitude complexes and axis deviations caused by cardiac position changes sometimes occur.


4. What is the recommended treatment for PPDH?

In symptomatic animals, therapy involves surgical closure of the peritoneal-pericardial defect after returning viable organs to their normal location. The presence of other congenital abnormalities and the animal’s clinical signs may influence the decision to operate. The prognosis in uncomplicated cases is excellent. Older animals without clinical signs may do well without surgery. Trauma to organs chronically adhered to the heart or pericardium during attempted repositioning is a potential concern in older animals.


5. In what ways can a structurally normal pericardium become diseased?

The accumulation of excess or abnormal fluid (effusion) is the most common pericardial disorder. Constrictive pericardial disease is recognized occasionally in dogs.


6. What types of fluid accumulate in the pericardium?

In dogs, most pericardial effusions are serosanguineous or sanguinous. The fluid usually appears dark red, with a packed cell volume of more than 7%, a specific gravity higher than 1.015, and a protein concentration between 3 and 6 g/dl. Mostly red blood cells are found on cytology, but reactive mesothelial, neoplastic, or other cells may be seen. The fluid does not clot unless the effusion resulted from very recent hemorrhage.


Transudates, modified transudates, and exudates are found occasionally. Pure transudates are clear, with a low cell count (less than 2500 cells/μl), specific gravity (less than 1.012), and protein content (less than 1 g/dl). Modified transudates may appear slightly cloudy or pink-tinged; cellularity is low but the specific gravity (1.015-1.030) and total protein concentration (2-5 g/dl) are higher than in a pure transudate. Exudates appear cloudy to opaque, or serofibrinous to serosanguinous. The white cell count (more than 15,000/μl), specific gravity (higher than 1.015), and protein concentration (more than 3 g/dl) are high. Cytologic findings are related to the cause.


7. Most pericardial effusions in dogs are hemorrhagic. What are the typical causes?

Dogs older than 7 years are likely to have neoplastic hemorrhagic effusion. Hemangiosarcoma is by far the most common neoplasm causing hemorrhagic pericardial effusion. Hemorrhagic pericardial effusion also results from various heart base tumors and pericardial mesotheliomas. Hemangiosarcomas usually arise from the right atrial wall, especially in the auricular area. Chemodectoma, arising from chemoreceptor cells at the base of the aorta, is the most common heart base tumor. Other heart base tumors also can occur, including thyroid, parathyroid, lymphoid, or connective tissue neoplasms. Pericardial mesotheliomas are uncommon but have been reported.


Idiopathic (so-called benign) pericardial effusion has been described most frequently in medium-to-large breeds of dogs. The German Shepherd, Golden Retriever, Great Dane, and Saint Bernard may be predisposed. Although dogs of any age can be affected, most are 6 years old or younger. Evidence of mild inflammation is common and pericardial fibrosis can result with time.


Other causes of intrapericardial hemorrhage include left atrial rupture secondary to severe mitral insufficiency, coagulopathy (e.g., warfarin-type rodenticides), and penetrating trauma (including iatrogenic laceration of a coronary artery during pericardiocentesis).


8. What conditions cause pericardial transudates and exudates?

Transudative effusions can be caused by congestive heart failure, pericardioperitoneal diaphragmatic hernia, hypoalbuminemia, pericardial cysts, or toxemias that increase vascular permeability (including uremia). Usually these conditions are associated with small volumes of pericardial effusion and cardiac tamponade is uncommon.


Exudates are rarely found in small animals. Pericarditis is unusual in association with systemic infections, but infectious pericarditis has been reported with actinomycosis, disseminated tuberculosis, Pasteurella multocida and other bacterial infections, coccidioidomycosis, and, rarely, systemic protozoal infections. Sterile exudative effusions have occurred with leptospirosis, canine distemper, and idiopathic benign pericardial effusion in dogs. Chronic uremia occasionally causes a sterile, serofibrinous, or hemorrhagic effusion in animals.


9. Does pericardial effusion always cause problems?

Unless intrapericardial fluid pressure rises to equal or exceed normal cardiac filling pressure, fluid accumulation within the pericardial space has little clinical consequence. When fluid accumulates slowly, the pericardium is able to distend and accommodate the increased volume while maintaining low intrapericardial pressure. As long as intrapericardial pressure is low, cardiac filling and output remain relatively normal. But, pericardial tissue is relatively noncompliant, so rapid fluid accumulation or large volume effusions cause intrapericardial pressure to rise quickly. Pericardial fibrosis and thickening further limit the compliance of this tissue. When intrapericardial pressure rises to and above normal atrial and venous pressures, cardiac filling is compromised. This is known as cardiac tamponade. Aside from the hemodynamic consequences of cardiac tamponade, very large pericardial effusions occasionally cause clinical signs from lung or tracheal compression (dyspnea and cough) or esophageal compression (dysphagia or regurgitation).


10. When is cardiac tamponade present?

Because the pericardium is relatively inelastic, there is a steep intrapericardial pressure-volume relationship when effusion accumulates quickly. Cardiac tamponade develops when intrapericardial pressure rises toward and exceeds cardiac diastolic pressure. This externally compresses the heart and progressively limits filling, causing cardiac output to fall. Eventually, diastolic pressures in all cardiac chambers and great veins equilibrate.


11. What are the consequences of cardiac tamponade?

Neurohumoral compensatory mechanisms of heart failure are activated when tamponade develops and cardiac output decreases. Signs of systemic venous congestion become especially prominent with time. Low cardiac output, arterial hypotension, and poor perfusion of other organs as well as the heart can ultimately lead to cardiogenic shock and death. The rate of pericardial fluid accumulation and the distensibility of the pericardial sac determine whether and how quickly cardiac tamponade develops. Rapid accumulation of even small volumes can markedly raise intrapericardial pressure, because the pericardium can stretch only slowly. The presence of a large volume of pericardial fluid implies a gradual process. Although cardiac contractility is not directly affected by pericardial effusion, reduced coronary perfusion during tamponade can impair both systolic and diastolic functions.


12. What clinical manifestations are characteristic of cardiac tamponade?

Clinical findings in animals with cardiac tamponade reflect poor cardiac output and right-sided (most commonly) congestive heart failure. Congestive failure arises from compensatory volume retention and the direct effects of impaired cardiac filling. Right-sided signs predominate because of the right heart’s thinner walls and low pressures, although signs of biventricular failure may occur. Nonspecific clinical signs such as lethargy, weakness, poor exercise tolerance, or inappetence may be noted before obvious ascites develops. Rapid accumulation of even small volumes of fluid (50-100 ml) can cause acute tamponade, shock, and death. In such cases, pulmonary edema, jugular venous distention, and hypotension may be evident without signs of pleural and peritoneal effusions or radiographic cardiomegaly.


Historical findings of weakness, exercise intolerance, abdominal enlargement, tachypnea, syncope, and cough are typical. Significant loss of lean body mass occurs in some chronic cases. Jugular vein distention or positive hepatojugular reflux, hepatomegaly, ascites, labored respiration, and weakened femoral pulses are common physical examination findings. A palpable decrease in arterial pulse strength during inspiration (pulsus paradoxus) might be discernable in occasional cases. 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. Heart sounds are muffled in animals with moderate-to-large pericardial effusions. Lung sounds are muffled ventrally with pleural effusion. Although pericardial effusion does not cause a murmur, concurrent cardiac disease may do so. Fever may be associated with infectious pericarditis.


13. What is pulsus paradoxus?

Cardiac tamponade causes an exaggerated respiratory variation in arterial blood pressure called pulsus paradoxus. Inspiration reduces intrapericardial and right atrial pressures, thereby facilitating right heart filling and pulmonary blood flow. Simultaneously, left heart filling is reduced because more blood is held in the lungs and the interventricular septum bulges leftward from the inspiratory increase in right ventricular filling; consequently, left heart output and systemic arterial pressure decrease during inspiration. The variation in systolic arterial pressure is usually higher than 10 mm Hg in animals with cardiac tamponade and pulsus paradoxus.


14. What is the role of radiography in the diagnosis of pericardial disease?

Thoracic radiography is useful for detecting the enlarged cardiac silhouette resulting from pericardial fluid accumulation. Massive pericardial effusion causes the “classic” round, globoid-shaped cardiac shadow (“basketball heart”) seen on both views. Other findings associated with tamponade include pleural effusion, caudal vena cava distension, hepatomegaly, and ascites. Pulmonary opacities compatible with edema and distended pulmonary veins are less frequently noted. Some heart base tumors cause deviation of the trachea or a soft-tissue mass effect. Metastatic lung lesions are common in dogs with hemangiosarcoma.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Pericardial Disease

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