Pericardial Disease



Pericardial Disease


Yaquta Kaka

Brent C. Lampert



INTRODUCTION

The pericardium is the site of many cardiac diseases that display classic physical examination signs and symptoms, imaging findings, and hemodynamic changes. These diseases include pericardial effusion, tamponade, pericarditis, and constrictive and effusive-constrictive pericarditis.


Anatomy and Physiology of the Pericardium

The pericardium (Figure 15.1) consists of two layers—a serous inner membrane and a fibrous outer sac—that surround the heart. The serous membrane forms the outer covering of the heart and is referred to as the visceral pericardium, whereas the thick fibrous sac covers the atria, ventricles, and proximal great vessels and is referred to as the parietal pericardium.1 As a mesothelial monolayer, the visceral pericardium adheres firmly to the epicardium and blends over the great vessels joining the parietal pericardium.2 The space between the parietal and visceral pericardium contains fluid and is called the pericardial cavity or sac. The pericardial space is defined by its attachment to the great vessels anteriorly, manubrium and xiphoid process ventrally, diaphragm caudally, and vertebral column dorsally.1 The space generally contains 50 cc of serous fluid that reduces the friction on the epicardium.1,2






The pericardial nerve fibers arise from the vagus, left recurrent laryngeal, and esophageal plexus along with the first dorsal ganglion and the stellate ganglion. Lymphatics are present on the parietal surface of the epicardium and drain into lymph nodes at the base of the heart,1 with the pericardial lymph having immunologic properties.3 Furthermore, the
pericardial membrane is active and assists with the transfer of water, electrolytes, and small molecules.

Two important functions of the pericardium include preventing displacement of the heart within the thorax and serving as a barrier to infection.1,3 It also helps with maintaining pressure differences within the different cardiac chambers. Mechanistically, the pericardium at times exhibits a restrictive function on the heart. At low stress, the pericardial tissue is flexible and can be easily stretched, and at the upper range of physiologic cardiac volumes, it becomes stiff. This is called the pericardial reserve volume. Once the pericardium reaches its reserve volume, further distention of the sac causes an increase in intrapericardial pressure, which is easily transmitted to the cardiac chambers resulting in coupling of the ventricles and atria.1,3,4 The pressure-volume curve of the pericardium is nonlinear: once the pericardial reserve is exhausted, small volume changes in the acute setting can cause dramatic increases in pressure and cardiac dysfunction (Figure 15.2).


PERICARDIAL EFFUSIONS

Pericardial effusions can occur because of a variety of causes, including excess production from an inflammatory state, damage to the cardiac chambers resulting in bleeding, decreased reabsorption because of increased systemic venous pressures in conditions such as decompensated heart failure, decreased lymphatic drainage from tumors or cancers, and lastly because of surgical manipulation of the area such as post-heart transplant.5,6,7

Most patients with pericardial effusions are asymptomatic, being discovered either on routine chest x-ray showing a globular shape to the heart or on transthoracic echocardiogram done for unrelated reasons.5 Pericardial effusions can be classified according to onset, location, hemodynamic effects, size, and composition (Table 15.1).5 Onset is defined as acute, subacute, or chronic. Location is circumferential, posterior, or loculated. Size is defined by echocardiographic measurement: small (<10 mm), medium (10-20 mm), and large (>20 mm) based on linear measurements of the largest echo-free space between the two layers of the pericardium at end diastole, and composition is transudative, exudative, chylous, pyopericardium, or hemopericardium.7






The etiology of pericardial effusions in developed countries is most often idiopathic (up to 50%) and in developing countries is tuberculosis, which has a mortality rate up to 40% in 6 months if untreated (Table 15.2).5,7 If suspected,
extracardiac screening should be performed, the pericardial effusion should be drained and analyzed, and a pericardial biopsy for culture and polymerase chain reaction (PCR) should be pursued.7 Other causes include cancer (10%-25%), infections (15%-30%), iatrogenic (15%-20%), and rheumatologic (5%-15%).















Pericardial effusions because of infections are usually exudative and, in some cases, present as pyopericardium. If infection is suspected, the pericardial effusion should be drained and sent for culture. In certain high-risk individuals, human immunodeficiency virus (HIV) and hepatitis C screening should also be pursued.7

Systemic diseases and metabolic changes can also lead to pericardial effusions. Uremia can cause an inflammatory effusion with fibrinous material in the pericardial sac. If uremic effusion results in pericarditis, the classic uremic pericardial rub may be audible. Primary treatment for this is hemodialysis.

Other systemic conditions such as hypothyroidism, severe malnutrition, and rheumatologic diseases can also lead to pericardial effusions. Primary treatment focuses on addressing the underlying condition.1,6,7

Hemopericardium can result from injury to cardiac structures or the great vessels from either blunt force/trauma or from systemic causes. Type A aortic dissection extending to the aortic root is one example.

Lastly, new-onset symptomatic large pericardial effusions can in some cases be the first manifestation of an underlying malignancy. Malignant effusions are usually transudative and hemorrhagic and more commonly associated with extracardiac cancers (lung, breast, lymphoma) as opposed to primary cardiac tumors. Patients with chest radiation and bone marrow transplant can also have pericardial effusions.1,7

Chylous effusions result from obstruction of pericardial lymphatic drainage. Hence, they may occur after cardiothoracic surgery or in association with congenital lymphangiomatosis. Other causes include chest trauma, mediastinal radiation, malignant neoplasm of the mediastinum, and thrombosis of the subclavian vein or superior vena cava.

Clinical features of a pericardial effusion vary based on the acuity and rapidity of fluid accumulation. With slow accumulation, the patient may have no symptoms. Classic symptoms of rapid accumulation or large effusions include dyspnea on exertion, chest fullness or tightness, and orthopnea. Additional symptoms include nausea, hoarseness, dysphagia from compression of surrounding structures, fatigue, palpitations, and fever. On physical examination, patients may be without findings unless there is pericarditis or hemodynamic compromise from tamponade.8,9

When a pericardial effusion is suspected, a transthoracic echocardiogram should be performed. An echocardiogram provides semiquantitative information regarding the hemodynamic effects of the effusion, size, and location. Generally, for uncomplicated effusions, echocardiogram is sufficient for diagnosis, and rarely other imaging modalities such as cardiac computed tomography (CT) or magnetic resonance imaging (MRI) are needed. Gated CT can be useful for delineating the effusion for surgical planning and estimating the composition based on Hounsfield units. Cardiac MRI like echocardiography has the ability to provide both hemodynamic and anatomic assessment of the fluid. However, unlike echocardiography it can also give insight into pericardial thickening and inflammation. Therefore, MRI can be useful in complicated cases or cases with inconclusive evidence via echocardiography.5,7,9

Management of pericardial effusion without hemodynamic compromise usually depends on the underlying etiology. Most cases (up to 60%) of pericardial effusion are associated with a known disease and the treatment is aimed at the underlying disease instead of the effusion itself. In idiopathic cases where there is concern for pericarditis, the patient should be treated as such with anti-inflammatory agents (see Acute Pericarditis, Treatment). In cases where there is no evidence of inflammation, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), or colchicine has not shown to be effective.

Pericardial effusions contributing to hemodynamic compromise (ie, cardiac tamponade, see below) should undergo urgent drainage for therapeutic (and possibly diagnostic) reasons. However, hemodynamically stable patients with a pericardial effusion do not require routine drainage or immediate drainage. Diagnostic sampling may be indicated if there is no clear etiology or when the results may alter subsequent management. The choice between percutaneous pericardiocentesis and surgical drainage depends on individual experience and specific clinical indications. Pericardiocentesis is the most common method and can be performed with echocardiographic or fluoroscopic guidance. Surgical drainage may be preferred for recurrent or loculated effusions or in cases where pericardial biopsy is needed for diagnosis.

Following pericardiocentesis, pericardial catheter is typically left in place for 24 to 48 hours or until the volume of drainage is less than 25 mL/day. Careful follow-up over days to weeks is important following pericardiocentesis to monitor for recurrence. For patients in whom pericardial fluid reaccumulates despite repeated pericardiocentesis, pericardiectomy can be considered.


Cardiac Tamponade

Cardiac tamponade is a life-threatening condition occurring when a pericardial effusion causes hemodynamic changes resulting in cardiac collapse. It is not necessarily dependent on the size of an effusion, as the rapidity of fluid accumulation also plays a role. If an effusion accumulates acutely, it can result in tamponade with only 200 cc of fluid. Conversely, a large effusion (>2 L) may result in no or minimal hemodynamic changes if it accumulates slowly, thereby allowing time for the pericardial sac to enlarge.

Under physiologic conditions, ventricular filling occurs with little interventricular dependence because of low pericardial pressures. Inspiration decreases pericardial pressure (because of reduced intrathoracic pressure) and increases system venous return to the right atrium (Figure 15.3). However, the decrease in intrathoracic pressure also causes decreased pulmonary venous pressure, resulting in a slight decrease in the
left ventricular (LV) preload and filling pressures. This in turn causes a slight decrease in LV stroke volume and systolic blood pressure (<10 mm Hg). In tamponade there is a substantial increase in pericardial pressure, which is directly transmitted to the cardiac chambers resulting in equalization of right ventricular (RV) and LV diastolic pressures. Therefore, during inspiration, the normal physiologic changes (such as a decrease in systolic blood pressure) are magnified resulting in substantial decreases in LV stroke volume. Furthermore, as the RV volume increases in inspiration, the interventricular septum bulges toward the left ventricle. This phenomenon is exaggerated in tamponade, further reducing LV stroke volume.7,10






Clinical features of a patient in tamponade include tachycardia, hypotension, muffled heart sounds, pulsus paradoxus, and increased jugular venous pressure. Electrocardiographic (ECG) signs of tamponade can include decreased QRS voltage with electrical alternans. These clinical features correlate with the hemodynamic changes. For example, the pulsus paradoxus results from the exaggerated decrease (>10 mmHg) of systolic blood pressure during inspiration, with the magnitude of the decrease correlating with the intrapericardial pressure.5,10

Echocardiography is the most useful diagnostic tool in a patient with suspicion for clinical tamponade. Echocardiogram can identify the size of the effusion, location, and assess for
hemodynamic effects. Echocardiographic features of tamponade include: swinging or rocking of the heart within the pericardium, right atrial late diastolic collapse, RV early diastolic collapse, exaggerated respiratory variation with tricuspid and mitral inflow on Doppler, and abnormal ventricular septal motion.5,6,10

The hemodynamic effects of tamponade are reversed by decreasing the pericardial pressure by draining the fluid via pericardiocentesis. Elective pericardiocentesis can be done with echocardiographic or fluoroscopic guidance. In an emergency, pericardiocentesis can be accomplished via a subxiphoid approach without imaging guidance. Pericardial fluid can also be drained surgically via a pericardial window or pericardiectomy. Surgical drainage is usually reserved for effusions that are more likely to reaccumulate, such as malignant effusions or in cases with localized effusions that are difficult to drain percutaneously. Following drainage of the effusion in tamponade, patients should have continuous telemetry monitoring and frequent vital sign measures for at least 48 hours. Echocardiogram should be done prior to hospital discharge to assess for any reaccumulation of fluid. Furthermore, follow-up echocardiograms should be considered within 1 to 2 weeks following discharge and again at 6 to 12 months to evaluate for recurrence or diagnose early constriction.


ACUTE PERICARDITIS


Pathogenesis and Epidemiology

Pericarditis is an inflammatory condition of the pericardium that can occur with or without an effusion. It can occur in isolation or because of systemic inflammatory conditions such as rheumatologic, metabolic, or secondary to cardiac injury. Acute pericarditis is the most common condition related to the pericardium. It accounts for ˜5% of emergency room visits for nonischemic chest pain and has been reported in ˜0.1% of admitted patients. The incidence of pericarditis is not completely known because of the lack of a gold standard way to diagnose pericarditis.11,12

The average age of patients with pericarditis is 40 to 60 years, with men having a twofold increased incidence compared to women. There are many different etiologies for pericarditis and the causes can be broadly divided into three categories: (1) infectious; (2) noninfectious; and (3) immune mediated.6

In general, pericardial inflammation occurs with thickening of parietal pericardium, causing edema with or without an exudative effusion and an increase in friction between the two layers.4 A small pericardial effusion is present in ˜60% of cases of pericarditis as seen on echocardiography, and approximately 15% of cases also have epicardial involvement as characterized by elevation in cardiac biomarkers.6,12

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Pericardial Disease
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