PERICARDIAL DISEASE (my class notes)

The pericardium is made up of two layers. The epicardium (visceral pericardium) is a serous membrane which lies directly adherent to the heart and the outer layer is called the fibrous (parietal) pericardium. The normal thickness of the parietal pericardium is approximately 2 mm. there is approximately 10 to 50 mL of fluid normally between the epicardium and the fibrous pericardium. This normal pericardial fluid may be seen as an echo-free space during ventricular systole. When the echo-free space persists throughout the cardiac cycle, a pericardial effusion is considered present. When quantitating the amount of pericardial fluid by echocardiography the fluid should be measure during ventricular diastole. Intrapericardial stands or fibrin strands within pericardial effusion most likely indicate inflammation or long-standing pericardial effusion.

The most common presenting symptom of acute Pericarditis is Chest pain; other symptoms include dyspnea, fever and cough. The chest pain associated with acute Pericarditis may be relieved by the patient sitting up and leaning forward.

The expected echocardiographic finding for Pericarditis is a pericardial effusion but patients may have Pericarditis without pericardial effusion (dry Pericarditis). Additionally pericardial effusion can occur in the absence of pericardial inflammation such as in post-operative cardiac surgery, chronic renal disease, collagen vascular disease, cardiac trauma, malignancy, AIDS and hypothyroidism.

The best guideline for differentiating pericardial effusion from pleural effusion by two dimensional echocardiography is: pericardial effusion is located anterior to the descending aorta; pleural effusion is present posterior to the descending aorta; in addition, a large pericardial effusion usually surrounds the heart.

Pulsus paradoxus is present when there is an exaggerated inspiratory decline in arterial blood pressure of more than 10 mmHg. Pulsus paradoxus is associated with cardiac tamponade for two reasons: filling of both ventricles against a common stiffness and respiratory changes in the venous pressure differential (systemic versus pulmonary) alternately favoring right and left ventricular filling. Respiratory variations of the cardiac Doppler signal of the atrioventricular valves suggest pulsus paradoxus.

In cardiac tamponade the right ventricular diastolic collapse occurs in early diastolic when the right ventricular volume and pressure are at lowest levels. Right ventricular diastolic collapse can be observed in the parasternal long axis view, parasternal short axis view, apical four chambers and the subcostal four chamber view.

With a large anterior and posterior pericardial effusion the heart may move freely within the pericardial cavity. This type of motion called the swinging heart syndrome tends to occur in large pericardial effusions. The swinging may cause the phenomenon of electrical alternant.

Marked (more than 25%) respiratory variation of tricuspid valve (increase in inspiration; decrease with expiration) and mitral valve (decrease in inspiration; increase with expiration) peak flow velocities and/or velocity time integrals is a strong indicator for the presence of cardiac tamponade. The orders in which changes occur are fairly predictable. Changes in the tricuspid occur first, followed by changes in the mitral valve with right atrial collapse being the next change and right ventricular diastolic collapse occurring last. Hepatic vein flow in cardiac tamponade mimics the flow changes of the tricuspid valve. The hepatic vein will have a reduction or reversal of diastolic flow expiration.

Constrictive Pericarditis results in the impairment of diastolic filling of the heart which may result in diastolic heart failure. Diastolic filling is impaired because of the constraint the pericardium places on the heart. Intracardiac filling pressures are usually increased in patients with constrictive Pericarditis. Constrictive Pericarditis should be a differential diagnosis in patients who present with congestive heart failure and normal global ventricular systolic function. Virtually all filling of the ventricle occurs in very early diastole. This abnormal pattern of diastolic filling is reflected in the characteristic dip-and-plateau (square root sign) waveforms in both the right and the left ventricles. The rapid rise in pressure after the early diastolic correspond to the period of rapid diastolic filling while the plateau phase correspond to the period of mid and late diastole when there is little additional expansion of ventricular volume. This can be expressed by the inflow patterns of the mitral valve and tricuspid valve with increased E/A ratio (more than 1.5) and shortened deceleration time ( less than 140 msec).

Causes of Constrictive Pericarditis include prior pericardiotomy, idiopathic, Pericarditis, radiation, infection and collagen vascular disease. Tuberculosis was at one time considered the leading cause of constrictive Pericarditis but idiopathic and prior pericardiotomy are the most common reason for Constrictive Pericarditis currently.

A thickened pericardium more than 2 mm, interventricular/inter-Atrial septal bounce (shudder), bound-down appearance of the ventricular walls with lack of pericardial slide, inferior vena cava plethora, normal Atrial dimensions, normal ventricular dimensions  and normal global ventricular systolic function are the echocardiographic findings associated with constrictive Pericarditis.

Pulsed wave Doppler in Constrictive Pericarditis:

Ø Mitral flow: restrictive pattern (increase E/A ratio, shortened DT)

Ø Increased peak velocity across the mitral valve with expiration

Ø Hepatic flow vein: expiratory flow decrease or reversal

Ø Tissue Doppler in mitral valve annulus is Normal E’ wave peak velocity (more or equal to 8 cm/s) and the E/E’ ratio is normal (more than 8), it is called annulus paradoxus