Pericardial effusion defines the presence of an abnormal amount and/or character of fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. Pericardial effusions can be acute or chronic, and the time course of development has a great impact on the patient's symptoms. Treatment varies, and is directed at both removal of the pericardial fluid and alleviation of the underlying cause, which usually is determined by a combination of fluid analysis and correlation with comorbid illnesses.
Image is from a patient with malignant pericardial effusion. Note the "water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.
In the human embryo, the pericardial cavity develops from the intraembryonic celom during the fourth week. The pericardial cavity initially communicates with the pleural and peritoneal cavities, but during normal development these are separated by the eighth week. Both the visceral and parietal pericardium are derived from the mesoderm, albeit from different parts of the embryo. The visceral pericardium develops from splanchnic mesoderm, as cells originating from the sinus venous spread out over the myocardium. The parietal pericardium derives from lateral mesoderm that covers and accompanies the developing pleuropericardial membrane, which will eventually separate the pleural and pericardial cavities. In healthy subjects, the pericardium covers the heart and great vessels, with the exception of only partially covering the left atrium.
Congenital absence of the pericardium can occur, and can be either partial or complete. It is often clinically silent, but can potentially lead to excessive cardiac motion (in the case of complete absence) causing vague chest pain or dyspnea, or, in case of partial absence with significant defects, strangulation of heart muscle and possible death.1
The pericardial space normally contains 15-50 mL of fluid, which serves as lubrication for the visceral and parietal layers of the pericardium. This fluid is thought to originate from the visceral pericardium and is essentially an ultrafiltrate of plasma. Total protein levels are generally low; however, the concentration of albumin is increased in pericardial fluid owing to its low molecular weight.
The pericardium and pericardial fluid provide important contributions to cardiac function.
The parietal pericardium contributes to resting diastolic pressure, and is responsible for most of this pressure in the right atrium and ventricle.
Through their ability to evenly distribute force across the heart, the pericardial structures assist in ensuring uniform contraction of the myocardium.
The normal pericardium can stretch to accommodate a small amount of fluid without significant change in intrapericardial pressure. However, once this pericardial reserve volume is surpassed, the pressure-volume curve becomes steep. With slow increases in volume, pericardial compliance can increase to lessen the increase in intrapericardial pressure.
Clinical manifestations of pericardial effusion are highly dependent upon the rate of accumulation of fluid in the pericardial sac. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 L without symptoms.
Understanding the properties of the pericardium can help predict changes within the heart under physiologic stress:
During hypervolemic states, the pericardium limits acute cardiac cavitary dilatation.
By distributing forces across the heart, the pericardium plays a significant role in the physiologic concept of ventricular interdependence, whereby changes in pressure, volume, and function in one ventricle influence the function of the other.
The pericardium plays a pivotal role in cardiac changes during inspiration. As the right atrium and ventricle fill during normal inspiration, the pericardium, by limiting the ability of these chambers to dilate, contributes to the bowing of the atrial and ventricular septums to the left. This reduces LV filling volumes, which lead to the drop in cardiac output. As intrapericardial pressures rise, this effect becomes pronounced, eventually leading to the finding of pulsus paradoxus (discussed below), heralding the development of pericardial tamponade.
The cause of abnormal fluid production depends on the underlying etiology, but it is usually secondary to injury or insult to the pericardium (ie, pericarditis). Transudative fluids result from obstruction of fluid drainage, which occurs through lymphatic channels. Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune processes within the pericardium.
Few large studies have characterized the epidemiology of pericardial effusion; however, the available data consistently shows that they are more prevalent than clinically evident.
A higher incidence of pericardial effusion is associated with certain diseases.
Small pericardial effusions are often asymptomatic, and pericardial effusion has been found in 3.4% of subjects in general autopsy studies.
A wide variety of malignant neoplasms and hematologic malignancies can lead to pericardial effusion. Data on the prevalence varies, with some studies showing the presence of pericardial effusion as high as 21% in such patients. A large study by Bussani et al showed cardiac metastases (9.1%) and pericardial metastases (6.3%) in cases of death from all causes in individuals with an underlying carcinoma at autopsy.2 Malignancies with the highest prevalence of pericardial effusion include lung (37% of malignant effusions), breast (22%), and leukemia/lymphoma (17%).
Patients with HIV, with or without AIDS, are also found to have increased prevalence of pericardial effusion.3 Studies have shown the prevalence of pericardial effusion in these patients to range from 5-43%, depending on the inclusion criteria, with 13% having moderate-to-severe effusion. The incidence of pericardial effusion in patients infected with HIV has been estimated at 11%; however, whether highly active anti-retroviral therapy (HAART) has influenced this number is unknown.
The mortality and morbidity of pericardial effusion is dependent upon etiology and comorbid conditions.
Idiopathic effusions are well tolerated in most patients. As many as 50% of patients with large, chronic effusions were asymptomatic during long-term follow-up.
Pericardial effusion is the primary or contributory cause of death in 86% of cancer patients with symptomatic effusions.
Survival rate for patients with HIV and symptomatic pericardial effusion is 36% at 6 months, 19% at 1 year.
No consistent difference among races is reported in the literature.
AIDS patients with pericardial effusion are more likely to be white.
No sexual predilection exists.
Observed in all age groups
Mean occurrence in fourth or fifth decades; earlier in patients with HIV3
A patient with pericardial effusion may report the following symptoms:
Chest pain, pressure, discomfort: Characteristically, pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine.
Upon examination, a patient with pericardial effusion may have the following signs:
Classic Beck triad of pericardial tamponade (hypotension, muffled heart sounds, jugular venous distension).
Pulsus paradoxus: Exaggeration of physiologic respiratory variation in systemic blood pressure, defined as a decrease in systolic blood pressure of more than 10 mm Hg with inspiration, signaling falling cardiac output during inspiration.
Pericardial friction rub: The most important physical sign of acute pericarditis may have up to 3 components per cardiac cycle and is high-pitched, scratching, and grating. It can sometimes be elicited only when firm pressure with the diaphragm of the stethoscope is applied to the chest wall at the left lower sternal border. The pericardial friction rub is heard most frequently during expiration with the patient upright and leaning forward.
Hepatojugular reflux: This can be observed by applying pressure to the periumbilical region. A rise in the jugular venous pressure (JVP) of greater than 3 cm H2 O for more than 30 seconds suggests elevated central venous pressure. Transient elevation in JVP may be normal.
Decreased breath sounds (secondary to pleural effusions4 )
Ewart sign - Dullness to percussion beneath the angle of left scapula from compression of the left lung by pericardial fluid
Gastrointestinal - Hepatosplenomegaly
Weakened peripheral pulses
The following are causes of pericardial effusion.
Idiopathic: In most cases, the underlying cause is not identified.
HIV infection can lead to pericardial effusion through several mechanisms, including the following:
Secondary bacterial infection
Malignancy (Kaposi sarcoma, lymphoma)
"Capillary leak" syndrome, which is associated with effusions in other body cavities
Viral: The most common cause of infectious pericarditis and myocarditis is viral. Common etiologic organisms include coxsackievirus A and B, and hepatitis viruses.
Pyogenic (pneumococci, streptococci, staphylococci, Neisseria, Legionella species)
Fungal (histoplasmosis, coccidioidomycosis, Candida)
Other infections (syphilitic, protozoal, parasitic)
Neoplastic disease can involve the pericardium through the following mechanisms:
Direct extension from mediastinal structures or the cardiac chamber
Retrograde extension from the lymphatic system
As mentioned previously, the most common cases of malignant effusion are lung, breast, lymphoma, and leukemia. However, patients with malignant melanoma or mesothelioma have a high prevalence of associated pericardial effusions.
Pericardial effusions are common after cardiac surgery. In 122 consecutive patients studied serially before and after cardiac surgery, effusions were present in 103 patients; most appeared by postoperative day 2, reached their maximum size by postoperative day 10, and usually resolved without sequelae within the first postoperative month. In a retrospective survey of more than 4,500 postoperative patients, only 48 were found to have moderate or large effusions by echocardiography; of those, 36 met diagnostic criteria for tamponade.5
Use of preoperative anticoagulants, valve surgery, and female sex were all associated with a higher prevalence of tamponade. Symptoms and physical findings of significant postoperative pericardial effusions are frequently nonspecific, and echocardiographic detection and echo-guided pericardiocentesis, when necessary, are safe and effective; prolonged catheter drainage reduces the recurrence rate.6
Pericardial effusions in cardiac transplant patients are associated with an increased prevalence of acute rejection.7
Other less common causes include the following:
Severe pulmonary hypertension
Acute myocardial infarction, including the complication of free wall rupture
Aortic dissection, leading to hemorrhagic effusion in from leakage into pericardial sac
Familial Mediterranean fever
Hypersensitivity or autoimmune related
Systemic lupus erythematosus8
Drug-associated (eg, procainamide, hydralazine, isoniazid, minoxidil, phenytoin, anticoagulants, methysergide)
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Jumat, 01 Januari 2010
Diposkan oleh FX di 10.06
The Holy Al-Qur'an (English version)
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- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome