Under heat stress, a decrease of the central venous pressure (CVP) was regularly observed, raising the question of whether this reaction is a limiting factor for the circulation. In animal experiments it could be shown, however, that despite a lowered CVP, which depended on the elevated body temperatures, a high cardiac output (CO), as well as an elevated stroke volume could be maintained. A low CVP went hand in hand with a low total peripheral resistance. It was argued that under these circumstances the low CVP was not limiting because the intrinsic factors of the heart (sympathetic stimulation) were capable of maintaining a high CO. In human experiments the lowered CVP had to be seen in relation to the degree of dehydration. Regardless of whether the plasma volume remained constant, as in exercise, or declined, as in thermal stress (sauna), the CVP followed the volume depletion of the vascular and extravascular space, and it might well be that under these circumstances CVP is limiting. In this case, however, the altered CVP must be seen first as a monitor for the fluid deficit and not as a factor controlling cardiac function.