Mechanical Effects Of The Pericardium

The degree to which the pericardium alters wall movement varies depending on the ratio of cardiac to pericardial size, loading conditions, and the degree of active and passive filling. Closure of the pericardial sac following open heart surgery has been proposed to (1) avoid possible postoperative complications, (2) reduce the frequency of ventricular hypertrophy, and (3) facilitate future potential reoperations by reducing fibrosis (1). Differences in ventricular performance dependent on the presence of the pericardium have been reported following cardiac surgery (2,3).

The presence of the pericardium physically constrains the heart, often resulting in a depressive hemodynamic influence that limits cardiac output by restraining diastolic ventricular filling (4,5). The physical constraint by the pericardium is translated into direct external mechanical forces that alter patterns in myocardial and systemic blood flow (5,6). Direct primary and indirect secondary effects are observed as additional forces through the free wall. Because both the left- and right-side atria and ventricles are bound by a common septum, geometrical changes from chamber interactions are dynamic, depending on the different filling rates and ejection rates of each of the four chambers (7,8). Thus, it is important to note that chamber-to-chamber interactions through the interventricular septum and by the pericardium further promote direct mechanical chamber interactions (9-11).

The effects of the pericardium on mechanical measures of cardiac performance are generally not evident until ventricular and atrial filling limitations are reached, i.e., changing geometrical and mechanical properties through factors such as maximum chamber volumes and elasticity. These effects become more evident as these pericardial limitations become extended (12,13). With the known force-length dependence of cardiac muscle, variation of chamber volumes through removal of the pericardium will influence isometric tension and therefore has a direct impact on systolic ejection. On the other hand, in specific cases when the restrictive role of the pericardium greatly increases, such as during cardiac tamponade, an increased intrapericardial fluid volume may result in critical restriction by the pericardium, which then clinically reduces cardiac performance (14).

It should also be noted that intrathoracic pressure creates an additional interaction between the ventricles, as well as between the heart and lungs in a closed chest. Thus, studying cardiac function in situ (with an opened chest) or in vitro allows elimination of the influences of intrathoracic pressures for identifying and quantifying pericardial influences on cardiac performance and ejection (15). Such isolation of pericar-dial effects from diastolic filling is necessary because normal ventricular output is dependent on diastolic pressure independent of the presence of the pericardium (16).

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