Some responses of the cardiovascular system to heat and fever.

This review outlines the mechanisms of body temperature control and the validity of various sites of measurement of core temperature. The mechanism of fever in response to circulating endotoxins are discussed, and the roles of various peripherally generated pyrogenic cytokines are outlined together with the loci of their action in the brain. The cardiovascular consequences of exposure to heat, particularly the pooling of blood in the skin and the increase of heart rate due to heating of the sinoatrial node, are discussed. The consequences of blood pooling, such as syncope or diminished G tolerance, are very important. Heat exposure and exercise lead to complex circulatory interactions, such as a higher heart rate for a given exercise load in the heat compared with a cool environment. At high work loads there may be a relatively lower cardiac output in hot conditions. Blood lactate levels and rectal temperature tend to be higher in exercise in the heat than exercise in the cold. Fever causes a large renal vasodilation and hepatic vasodilation, which are humorally mediated and which effectively cause a splanchnic vascular shunt of some consequence if there is already heart failure or shock. Syncope during fever, endotoxin shock and the role of pyrogens in heat stroke are discussed.