EFFECTS OF NERVE STIMULATION AND HORMONES ON THE HEART 



541 



C ASPHYXIA AFTER 



ANESTHETIC AND 



THORACOTOMY 



mm 

 50- 



LEFT VENTRICULAR DIAMETER 



■ r. ! 



r^> 



47^Y y ^ ^ ^ 



Maximum 

 Diometer 



mm 



Hg LEFT VENTRICULAR PRESSURE 'x 

 120- . -^ n ,r« ^ /^' 



D PASSIVE TILTING E PASSIVE TILTING 



^->» 



40- 



mm 

 Hg 



o- 



LEFT VENTRICULAR DIASTOLIC PRESSURE 



/ ^ 



FIG. 5. When a dog reclines, left ventricular diameter increases progressisely until the diastolic 

 diameter begins to display a plateau (diastasis). After anesthesia and thoracotomy, the heart was 

 observed to distend to a maximal size during asphyxia, and this maximum distention is comparable 

 to the diastolic dicm:ieter in the reclining dog. The reduction in ventricular dimensions is not a 

 result of the muscular activity because it occurs with passi\e tilting with the head up but not so 

 obviously with tilting head down. 



of blood in the lungs and heart is depleted. Kjellberg 

 et al. (21) made .several observations indicating that 

 the left ventricle is a major source of the blood given 

 up by the heart in this type of redistribtition. 

 Duomarco et al. (8) presented evidence that the 

 venae cavae and their intrathoracic branches are 

 all well distended when normal men are recumbent. 

 In the erect posture the superior vena cava and its 

 branches are distinctly collapsed above a level just 

 above the right atrium. The depletion of blood from 

 the superior vena cava, brachiocephalic vessels, and 

 pulmonary veins in erect men represents a reduction 

 in the capacity of the \enous reservoirs just upstream 

 from both ventricles. Thus the atria and the adjacent 

 venous channels correspond in some ways to the 

 venous reservoir in the heart-lung preparation and 

 may be regarded as a low pressure sump from which 

 the ventricles fill during each diastolic interval. 



The Preventricular Sump 



The blood that enters a ventricular chamber during 

 each diastolic filling period comes not only from the 



corresponding atrium but also from considerable 

 distances along the venous channels leading to the 

 heart. Thus, the central veins and atria represent low 

 pressure, variable capacity sumps just upstream from 

 the right and left ventricular cavities. This concept 

 of a preventricular sump corresponds to the "surge 

 chamber" proposed by Sjostrand (44) and elaborated 

 by Holmgren (18). An abrupt increase in heart rate 

 can produce a transient increase in cardiac output 

 without a corresponding acceleration of venous flow 

 by pumping out some of the ventricular systolic 

 reserve capacity and by depleting some of the capacity 

 of this sump. The augmented cardiac output can 

 persist only for a few beats, however, if the venous 

 inflow does not increase promptly. Thus, it is neces- 

 sary to visualize a very prompt acceleration of blood 

 flow in all parts of the circulatory tree during any 

 transition from one level of cardiac output to another. 

 In standing human subjects, the collapse of the 

 superior vena cava and the transfer of blood out of 

 the pulmonary veins reduces the capacity of the 

 preventricular sumps of the right and left ventricles, 

 respectively. On this basis, cardiac output is more 



