79 2 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



bility, pliability, and limited anchorage [see Pfuhl, 

 (129) and Nelemans (118)]. A number of additional 

 functions have been ascribed to the pericardium, 

 namely : protection of the entire heart from over- 

 dilatation; protection from overdilatation of the left 

 ventricle only; protection from overdilatation of the 

 right ventricle only; increase of cardiac performance 

 because of higher filling pressure; better harmonic 

 coordination of right and left ventricular contrac- 

 tions; facilitation of atrial filling; and facilitation of 

 the gliding of the epicardium through lymph lubrica- 

 tion. 



Most experimental studies on the function of the 

 pericardium concern abnormal situations such as 

 are met in pericardial effusion and tamponade 

 from various other causes [Feinberg (46), Adcock 

 et al. (1), Evans et al. (44), Nerlich (119), Metcalfe 

 et al. (112), Isaacs et al. (84), Bencini & Parola 

 (9)]. The information from these studies, though in 

 some respects limited to abnormal hemodynamic 

 situations, has contributed much to the elucidation 

 of normal functions of the pericardium. 



Since some of the functions are implicit from the 

 architecture of the pericardium, a brief anatomical- 

 histological review will be helpful (118). The parietal 

 pericardium, generally just called pericardium, 

 forms a thin, but firm sac of connective tissue en- 

 veloping the ventricles and atria. At the base of the 

 heart, near the entry of the veins into the atria, 

 the parietal pericardium joins the visceral pericar- 

 dium or "epicardium." Pericardium and epicardium 

 are separated by a thin fluid film of pericardial 

 liquor which is similar to the fluid filling the intra- 

 pleural space. The outer aspect of the pericardium 

 is covered with a thin layer of loose connective tissue 

 which constitutes the pericardial, or parietal, pleura. 

 The pericardium is attached to the diaphragm with 

 two septa (right and left) to the sternum and to the 

 mediastinum. This anchorage limits the mobility of 

 the sac and in turn confines the heart to a definite 

 space within the thorax, especially in primates. 



Histologically the pericardium consists of three 

 layers of regularly oriented collagenous and elastic 

 fibers, each oriented in a different direction. The 

 fibers of the outer and middle layer form a thicker 

 structure than those of the inner layer. In a prepara- 

 tion which is not submitted to stretch, the collage- 

 nous fibers appear wavy and the elastic fibers appear 

 straight. Nelemans (118) showed that with an acute 

 dilatation of the normal heart, the pericardium 

 extends itself by approximately 20 per cent until 

 the elastic fibers are markedly stretched and the 



120 



150 VOLUME (ml) 300 



fig. 25. Pericardial pressure-volume curve in a dead dog, 

 determined after removal of heart. The volume of the heart 

 is replaced by fluid injected into the pericardial space. [From 

 Holt (78).] 



rather tense collagenous fibers hinder further ex- 

 pansion. This elastic stretching is quickly reversible, 

 since the sac will again fit snugly when cardiac dila- 

 tation is abrogated. If, however, the heart dilates 

 beyond the limit of elastic stretch, which obviously 

 can only happen if venous return and end-diastolic 

 pressures rise substantially, then the pericardium 

 will "give" or yield. However, this additional stretch- 

 ing is not quickly reversible and persists for a long 

 time after the heart has returned to its normal shape, 

 as evidenced by the slackness of the pericardial sac. 

 The additional stretching is of "plastic" nature and 

 can be attributed to the collagenous fibers which 

 return only very slowly to their previous length 

 after stretching. This dual mechanism of "elastic" 

 and "plastic" stretch hinders acute overinflation 

 (elastic limitation) but permits long term dilatation 

 of the heart (plastic adaptation). 



Nelemans' (118) views concerning the "plastic" 

 behavior of the pericardium are supported by ob- 

 servations made in experimental pericardial effusion : 

 following the infusion of 50 ml of saline into the peri- 

 cardial sac in an open-chest dog, the mean intra- 

 pericardial pressure first rises markedly but then 

 gradually decreases to a lower level. Withdrawal 

 and immediate reinfusion of the same amount of 

 fluid results in a lower pressure than the one initially 

 obtained. Withdrawing the saline, but then waiting 

 for about 2 hours before reinjecting it, results in 



