A. Definition. There is a wide spectrum of pericardial disease seen in critical care, but the clinicopathologic processes involved are relatively few and include the following:

1. Pericarditis, with or without pericardial effusion and with or without myocardial involvement (myopericarditis).

a. Acute.

b. Subacute.

c. Chronic, fibrinous, noneffusive, or exudative.

2. Pericardial effusion and cardiac tamponade.

3. Constrictive pericarditis.

a. Acute.

b. Subacute.

c. Chronic adhesive.

d. Fibrocalcific.

1. The pericardium is a double-layered fibroserous sac that surrounds the heart and is made up of a visceral layer that adheres firmly to the epicardium and a tough, fibrous outer parietal layer.

2. Importantly, the pericardium reflects over the origin of the great vessels; therefore, a hemorrhagic pericardial effusion may develop with ascending aortic dissection/rupture.

3. A small amount of fluid (up to 50 mL) normally exists between these two pericardial layers in the pericardial space, and there is enough slack in the parietal pericardium to usually accommodate 100 to 200 mL of fluid before causing hemodynamic compromise.

4. Histologically, the pericardium is made up of compact collagen layers interspersed with elastin fibers, which help provide mechanical viscoelastic function.

1. Idiopathic.

2. Infectious (viral or bacterial).

3. Related to myocardial infarction.

4. Secondary to connective tissue disease/vasculitis.

5. Immunopathic or associated with “hypersensitivity” states including post cardiotomy related.

6. Secondary to diseases of contiguous structures.

7. Secondary to disorders of metabolism.

8. Neoplastic.

9. Traumatic.

10. Radiation induced.

11. Uremic.

1. The unique anatomy of the pericardium allows for the pressure-volume relation of the pericardium to be nonlinear, with an initially flat response (little change in pressure despite large changes in volume) and a subsequent “threshold” critical volume at which point a steep slope develops (large change in pressure with small changes in volume).

2. The pericardium serves several important functions although it is not essential for life and its congenital absence or surgical removal leads to no major clinical problems.

a. The pericardium limits distention of the cardiac chambers.

b. This facilitates interaction, interdependence, and coupling of the ventricles and atria such that changes in pressure/volume in the right heart influence pressure/volume in the left heart and vice versa.

c. The normal thin-walled right ventricle is usually affected more by this restraint than is the thick-walled left ventricle.

3. Excessive fluid in the pericardium increases the normal pericardial effect on ventricular interaction and exaggerates the normal inspiratory decrease in systemic blood pressure, thereby leading to pulsus paradoxus (inspiratory drop in blood pressure >10 mm Hg).

4. Although pulsus paradoxus is the hallmark of tamponade, it can be seen in other disorders, including obstructive lung disease (including severe asthma), pneumothorax, pulmonary embolism, tense ascites, obesity, mitral stenosis with right heart failure, right ventricular infarction, hypovolemia, and cardiogenic shock.

5. Beyond pericardial stretch, compensatory mechanisms for tamponade are mainly adrenergically mediated, including tachycardia, peripheral vasoconstriction, and maintained ejection fraction (in pure tamponade without heart disease, the ejection fraction is normal or increased); eventually, these compensatory mechanisms fail and cardiac output or stroke volume fall.

6. Like tamponade, constriction severely limits ventricular filling, with equalization of left and right heart diastolic pressures; systolic right ventricular pressure rises but usually to <50 mm Hg, and the ratio of right ventricular end-diastolic pressure to systolic pressure is usually >0.3.

7. Unlike in cardiac tamponade, the heart is not compressed in early diastole and relaxes normally or abruptly (rubber bulb effect) as filling proceeds until it reaches its pericardial limit.

1. Acute pericarditis may be asymptomatic, but more often the patient has central, sharp, positional (worse when patient is supine and reduced
when patient sits up) chest pain with a pleuritic component; however, chest pressure that may approximate angina may also occur.

2. Chest pain may migrate to anywhere in the chest but frequently radiates to one or both of the trapezius ridges.

3. True dyspnea does not occur in the absence of a large pericardial effusion, but shallow, rapid breathing due to pleurisy is often present.

4. Odynophagia (pain on swallowing) occasionally occurs.

5. The pericardial friction sound (rub) is pathognomonic but varies from faint to very loud (especially in uremic pericarditis) and may be transient; a fully developed rub has three components: atrial late diastolic rub, ventricular systolic rub, and an early diastolic rub.

6. The white blood cell count, sedimentation rate, and other acute phase reactants vary according to the etiologic agent or primary illness; serum levels of cardiac enzymes vary, depending on coexistent myocardial involvement (myopericarditis).

7. Acute pericarditis is most often an inflammatory, fibrinous disease without an increase in the normal amount of pericardial fluid; cardiomegaly on chest radiography will occur only if >200 to 250 mL of pericardial fluid has accumulated.

8. Typically, four potential electrocardiographic (ECG) stages are noted, with the entire ECG evolution occurring in a matter of days or weeks.

a. Stage I (Fig. 28-1): diffuse concave upward ST (J-point) elevation with ST depression in lead AVR consistent with epicardial inflammation.

b. Stage II: ST (J) segments return to baseline more or less “in phase,” with little change in T waves. The PR segments may be depressed in either stage I or, more often, stage II and rarely in stage III. T waves progressively flatten and invert in all or most of the leads that showed ST segment elevations.