Epidemiology: one of the most common etiologies of constrictive pericarditis in developed countries
Physiology
Normal Anatomy of the Pericardium
Inelastic Structure Around the Heart and Portions of the Great Vessels
Pericardial Layers
Parietal Pericardium: more fibrous layer
Visceral Pericardium: adherent to the epicardium
Pericardial Layers are Separated by a Potential Space: which normally contains <50 ml of fluid
Pericardial is Approximately 2-3 mm Thick
Pericardium Accommodates Slow Filling, But is Poorly Tolerant of Rapid Filling of the Pericardial Space
Pericardium is Attached to the Sternum and Diaphragm
Normal Functions of the Pericardium
Barrier to Inflammatory Disease
Maintenance of Normal Position in the Chest
Limitation of Acute Myocardial Distention
Enhancement of Normal Interaction of the Ventricles
Pericardial Thickening
Definition: pericardial thickness >4 mm is considered abnormal
Hemodynamic Consequences of Non-Compliant, Thickened Pericardium
Uniformly Increased Filling Pressures in All Cardiac Chambers
Decreased Preload with Decreased Stroke Volumes
Increased Ventricular Interdependence Via Increased Septal Interactions: results in characteristic “septal bounce”
Loss of Normal Respiratory Transmission of Intrathoracic Pressure Changes to the Cardiac Chambers: in the normal state, the intrathoracic pressure decreases about 5-10 mm Hg during inspiration and this pressure change is fully transmitted to the cardiac chambers
Exaggerated Respiratory Variation in Both Inflow Velocity and Ventricular Filling: since the extrapericardial components of the vena cava and the pulmonary veins are still subjected to these intrathoracic pressure changes
Abnormal Mitral and Tricuspid Inflow Velocities: good sensitivity/specificity for constrictive pericarditis (although there is some overlap with pericardial tamponade)
In Both Tamponade and Constrictive Pericarditis, Mitral Inflow Velocity Decreases After Inspiration and Increases After Expiration
In Both Tamponade and Constrictive Pericarditis, Tricuspid Inflow Velocity Increases After Inspiration and Decreases After Expiration
Cardiac Catheterization Allows Differentiation of Constrictive Pericarditis from Restrictive Cardiomyopathy
Stroke Volume is Almost Always Decreased in Constrictive Pericarditis: due to decreased diastolic filling
Findings
Pulmonary Artery Pressure and RV Systolic Pressures are Frequently Increased with Restrictive Cardiomyopathy: may be present also in constrictive pericarditis
Equalization of End-Diastolic Pressures in the Cardiac Chambers
Increased Atrial Pressure with Prominent x and y-Descents
Dip-and-Plateau (Square Root Sign) if Ventricular Diastolic Pressure
Clinical Manifestations
Cardiovascular Manifestations
General Features
Atrial Arrhythmias: occur in 16% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Elevated Jugular Venous Pressur (JVP): occurs in 93% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Rapid x and y-Descents
Kussmaul’s Sign (see Kussmaul’s Sign): occurs in 21% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Rise in the Jugular Venous Pressure on Inspiration
Kussmaul Sign May Occur in Any Etiology of Severe Right-Sided Heart Failure or Right Ventricular Infarction
Low QRS Voltage (see Electrocardiogram): occurs in 27% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Pulsus Paradoxus (see Pulsus Paradoxus): occurs in 19% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Defined as a >10 mm Hg Drop in Systolic Blood Pressure Upon Inspiration
Pulsus Paradoxus May Also Occur in Pericardial Tamponade, SVC Obstruction, Asthma, Obstructive Airways Disease, Pulmonary Embolism, and Cardiogenic Shock
Pericardial Calcification on Chest X-Ray (CXR): occurs in 25% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Pericardial Rub: occurs in 16% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Pericardial Knock or Third Heart Sound: occurs in 47% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Early, High Pitched Third Heart Sound
Sudden Inspiratory Splitting of the Second Heart Sound: may occur
Features Characteristic of Fluid Overload-Type Presentation
Anasarca
Peripheral Edema (see Peripheral Edema): occurs in 76% of cases (Nat Rev Cardiol, 2014) [MEDLINE]
Features Characteristic of Low Cardiac Output-Type Presentation
Mechanism: hepatic vein pressures are typically higher in constrictive pericarditis than those in other etiologies of right-sided congestive heart failure -> increasing probablity of developing hepatic necrosis (and ultimately cardiac cirrhosis)
ClinicalPleural Effusion: although may be left, right, or bilateral, studies suggest that effusions associated with pericardial disease are more common on the left (NEJM, 1983) [MEDLINE]
