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The principal reason for hypothermic CPB is to protect the heart and other organs by reducing metabolic rate and thus oxygen requirements. In the myocardium, hypothermia sustains intracellular reserves of high-energy phosphates and preserves higher intracellular pH and electrochemical neutrality. Myocardial cooling can be achieved with cold cardio- plegia, pouring cold topical solution on the heart and cooling jackets, as well as by systemic hypothermia. Systemic hypothermia is not uniform due to different blood flow to different vascular beds. High blood flow rates and slow cooling ensures less variation in systemic hypothermia. Temperature should be measured at multiple sites and the advantages and limitations of each site needs to be recognized. During cardiac surgery temperature can be measured in the following locations: nasopharynx, tympanic membrane, pulmonary artery, bladder or rectum, arterial inflow, water entering heat exchanger, and venous return. Nasopharyngeal temperature probes underestimate, but approximate to brain tempera- ture, with the mixed venous temperature on the CPB circuit being an approximation of average body temperature. Bladder and rectal temperatures give an indication of core body temperature, but these can be erroneous due to interference from varying urine production and fecal matter, respectively. These low blood flow sites tend to underestimate temperature so are particularly valuable following deeper levels of hypothermia. On re-warming the aim is to achieve uniform normothermia. To avoid rebound hypothermia after cessation of CPB, which occurs if too great a temperature gradient is allowed to develop between peripheral and core temperatures, vasodilators can be used to promote more uniform re-warming by distributing greater blood flow, and therefore heat, from the core to peripheries. The process of re-warming must be controlled to avoid rapid changes in temperature, or excessive blood temperatures, which can result in microbubble formation due to the reduced solubility of gases in blood as the temperature increases, denaturing of plasma proteins, hemolysis, and cerebral injury. As a general guide for every 1°C drop in temperature there is an associated 7% drop in oxygen demand, i.e. a 7°C reduction in temperature results in a 50% drop in oxygen demand (see Table 5.6). At < 15°C oxygen is too tightly bound to hemoglobin and is therefore unavailable to tissues. In addition, the viscosity of the blood can be too high for effective flow through the CPB circuit.