Pericardial disease can be divided into constrictive pericarditis and effusive pericarditis. Constrictive pericarditis involves thickening of both the fibrous and serous layers of the pericardium. Effusive pericarditis is the accumulation of fluid within the pericardial sac. Both entities are the result of inflammatory processes, may present acutely or have a chronic course, and produce a varying degree of cardiac compression.
A. Acute Tamponade
· Pericardial pressure is normally subatmospheric and becomes more negative during inspiration
· Transpericardial pressure is highest at end diastole, when ventricular volume is greatest
· The pressure-volume curve for the pericardium rises steeply after a certain volume is exceeded, so that removal of small amounts of fluid will result in significant reduction in pressure
· A rapid increase in intrapericardial fluid produces acute tamponade, with pressures reaching 20-30 mmHg
· Systemic venous pressure rises, heart volumes are reduced, and systemic arterial pressure falls = Beck's triad
· This compression also causes pulsus paradoxus, which is a decrease in arterial pressure of more than 10 mmHg during inspiration
· The x descent is accentuated, but the y descent is flattened or absent, as cardiac filling is severely restricted during diastole
B. Chronic Constrictive Pericarditis
· The fibrous envelope reduces end-diastolic volume and causing inadequate preload
· The right ventricular pulse wave during diastole demonstrates an early drop followed by a high plateau = square-root sign
· Mean venous pressure is elevated and the x and y descents are steep and deep
· Pulsus paradoxus is infrequent and may be difficult to detect in the setting of atrial fibrillation
· Systolic left ventricular function is preserved, but the heart may still have impaired contractility
C. Chronic Effusive Pericarditis
· The increased fluid volume presents initially as acute tamponade
· Pericardial fluid drainage, however, does not resolve the compression, as the thickened pericardium continues to restrict diastolic filling
· Like chronic constrictive pericarditis, the y descent is steep and deep, and pulsus paradoxus is infrequent
A. Morphology
· Inflammation affects both the parietal and visceral pericardium
· The pericardial space accumulates both fluid and fibrinous deposits
· Both layers of the visceral pericardium eventually fuse, and the heart is surrounded by a thick fibrous envelope
· This entire process may calcify and become adherent to the underlying myocardium
B. Etiology
· In most patients, the underlying cause is unknown
· 10% have progression of acute pericarditis
· Less than 5% of cases are the result of cardiac surgery, and the time interval is widely variable
· Other causes include mediastinal radiation, rheumatoid disease, sarcoidosis, tuberculosis, and trauma
C. Natural History
· Factors affecting disease progression and development of symptoms are incompletely known
· Atrial fibrillation is a common occurrence and causes sudden clinical deterioration
· When ascites is present, progression is more rapid
· Symptoms are classically delayed for several years after the initial episode of acute pericarditis
· Fatigue, dyspnea on exertion, and jugular venous distension are early symptoms
· Hepatomegaly, ascites, and peripheral edema are late findings, but dyspnea at rest and orthopnea are not common
· On examination, there may be systolic retraction and a pericardial knock (produced by rapid ventricular filling in early diastole
· Protein-losing enteropathy may be present, with severe hypoproteinemia
· CXR demonstrates pericardial calcification in about 40% of patients and suggests compression in about 60%
· EKG will show non-specific ST-T changes in the majority of patients; some will have a low QRS voltage or atrial arrhythmia
· Echocardiography is most useful in acute tamponade, but can be helpful in assessing restrictive disease
· CT and MRI can identify thickened pericardium, but give little additional information
· Catherization characteristically shows equal end-diastolic pressures in the right atrium, pulmonary artery, and left atrium
· Rapid infusion of volume can reproduce these features if catheterization findings are equivocal
· A small anterolateral thoracotomy for pericardial biopsy can be used to distinguish between constrictive pericarditis and restrictive cardiomyopathy
· Diagnosis is a general indication
· Patients with minimal physiologic alteration and serious concomitant disease may be delayed until more significant pericardial symptoms develop
· Patients with radiation-induced pericarditis should only undergo operation when symptoms are advanced
A. Left anterolateral thoracotomy
· Dissect off phrenic nerve and incise pericardium through area of minimal calcification over left ventricle
· Create longitudinal incision anteriorly and posteriorly
If a pericardial space is present:
· An anterior pericardial flap is developed as far as the right AV groove and resected
· A posterior flap is developed far posteriorly and excised
· Care must be taken to resect bands off the pulmonary trunk to prevent postoperative RV hypertension
· Any fibrous plaques adherent to the eipcardium are now resected
· If the epicardium is thin, it should not be disturbed; if thickened, it should be either removed entirely or in a number of areas
If no pericardial space is present:
· Deepen the longitudinal incision over an area of myocardium
· Carefully dissect flaps, leaving islands of scar and calcification attached to the myocardium where dissection is not possible
· Retain long flaps until dissection is complete to help control bleeding
· Care must be taken over the coronary vessels, and plaques may be left undisturbed here
B. Median sternotomy
· Cardiopulmonary bypass may be used and may be most convenient through the femoral vessels
· The pericardium is opened vertically and flaps dissected in a similar manner
· The pericardial flaps are excised about 1 cm anterior to the phrenic nerves, and dissection resumed posterior to the nerves
· The outer pericardial layer may then be seperated from the pleura which contains the phrenic nerves
· Hospital mortality is about 5%
· Most early deaths are from acute cardiac failure
· 1-year, 5-year, and 10-year survival is about 90%, 75%, and 65%
· Most late deaths are from chronic heart failure
· Risk factors for death include poor preoperative functional status, ascites, peripheral edema, and previous radiation
· Most patients have good results for functional status and reoperation is very infrequent
A. Morphology
· Inflammation causes secretion of excessive amounts of fluid as well as fibrin
· Strands of fibrin may accumulate within the layers, known as "bread and butter" pericarditis
· Both layers may be thickened and adherent
· The fluid may be loculated
B. Etiology
· Common underlying diseases included advanced renal disease, dialysis, malignancy, and trauma
· The exact mechanisms are unknown
· Infection is rarely the cause of effusive pericarditis
· It is more common in young women
C. Natural History
· Effusive pericarditis occurs in about 15% of patients on hemodialysis, and tends to occur early
· The course from malignancy is unpredictable
· The long-term course is unknown
· Some patients present with fever, elevated white blood cell count, and a pericardial rub
· Others may have chest pain ranging from mild to severe
· Few patients develop acute tamponade
· Clinical examination demonstrated jugular venous distension; Beck's triad and pulsus paradoxus may or may not be present
· CXR may demonstrate the classic enlarged, globular cardiac silhouette
· EKG shows widespread ST elevation when the effusion is acute; in chronic effusion, the EKG findings are similar to those of constrictive pericarditis
· Echocardiography is very accurate in the diagnosis and allows ultrasound-guided aspiration
· Pericardial window is indicated for acute tamponade or when significant symptoms do not resolve after 7-10 days of intensive medical therapy
· Subtotal or total pericardiectomy is indicated when effusion recurs or cannot be drained satisfactorily
A. Pericardiocentesis
· Echocardiographic guidance is safe and effective
· Drainage of loculations may be difficult
B. Subxiphoid Pericardial Window
· Perform 4-8 cm vertical midline incision over xiphoid process and upper abdomen
· Remove or retract xiphoid process upward and dissect diaphragm off undersurface of sternum
· Open pericardium, aspirate fluid and excise a large portion of the pericardium
· Insert suction drain and close wound loosely
C. Left Anterolateral Pericardial Window
· Perform small anterolateral thoracotomy
· Create window anterior to the phrenic nerve
D. Subtotal/Total Pericardectomy
· See #5 above for chronic constrictive pericarditis
· Long-term survival is considerably lower in patients who have underlying malignancy than with other diseases
· Relief of symptoms is generally excellent
· Pericarditis indicated if the effusion is not loculated
· Recurrent effusions should be treated with pericardial window
· Loculations or development of continued sepsis are indications for pericardectomy
· Medical therapy alone is sufficient when the effusion is moderate and there is minimal pericardial thickening
· Pericardial window is indicated for persistent effusion, recurrent effusion after aspiration, thickened pericardium, or signs of pericardial constriction
· Development of chronic constrictive pericarditis is an indication for pericardectomy