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Severe hypothermia may be induced deliberately to confer protection against tissue ischemia, specifically during cardiac surgery and occasionally during neurosurgery. Drugs such as barbiturates and volatile anesthetics provide considerably less protection than even mild hypothermia does.[99] Because many organs compensate poorly for hypothermia, temperatures as low as those deliberately induced are usually lethal when unintentional. Deliberate hypothermia is safe only because anesthesiologists understand and treat the physiologic changes caused by core temperatures 10°C to 15°C below normal.
Although deep hypothermia (i.e., 28°C) has been used to facilitate cardiopulmonary bypass for decades, recent evidence suggests that hypothermia is either unhelpful or simply harmful. For example, hypothermia may be associated with prolonged ventricular dysfunction[188] and does not limit cognitive impairment after bypass.[189] Furthermore, normothermia appears to improve major outcomes after bypass surgery. [190] Consequently, cardiac surgery is increasingly performed at either "tepid" temperatures (i.e., 33°C) or normothermia.
Ischemia damages tissues because oxygen deprivation forces cells to obtain energy anaerobically. Because this mechanism is inefficient, it may not provide adequate energy. Anaerobic metabolism also produces more toxic metabolic waste products (e.g., lactate and superoxide radicals) than the Krebs cycle does, which is particularly serious when these waste products are not removed by circulating blood.
Hypothermia decreases the whole-body metabolic rate by approximately 8%/°C to approximately half the normal rate at 28°C. Whole-body oxygen demand diminishes, and oxygen consumption in tissues that have higher than normal metabolic rates, such as the brain, is especially reduced. Low metabolic rates allow aerobic metabolism to continue during periods of compromised oxygen supply; toxic waste production declines in proportion to the metabolic rate. Although a decreased metabolic rate certainly contributes to the observed protection against tissue ischemia, other specific actions of hypothermia (including "membrane stabilization" and decreased release of toxic metabolites and excitatory amino acids) may be most important.
Cerebral blood flow also decreases in proportion to the metabolic rate during hypothermia because of an autoregulatory increase in cerebrovascular resistance. The arteriovenous PO2 difference thus remains constant, and the venous lactate concentration does not increase. Cerebral function is well maintained until core temperatures reach around 33°C, but consciousness is lost at temperatures below 28°C. Primitive reflexes such as the gag, pupillary constriction, and monosynaptic spinal reflexes remain intact until approximately 25°C. Nerve conduction decreases, but peripheral muscle tone increases, and rigidity and myoclonus ensue at temperatures near 26°C. Somatosensory and audio evoked potentials are temperature dependent, but not significantly modified at core temperatures of 33°C or higher.
Hypothermic effects on the heart include a decrease in the heart rate, increased contractility, and well-maintained stroke volume.[191] Cardiac output and blood pressure both decrease. At temperatures below 28°C, sinoatrial pacing becomes erratic and ventricular irritability increases. Fibrillation usually occurs between 25°C and 30°C, and electrical defibrillation is generally ineffective at these temperatures. Because coronary artery blood flow decreases in proportion to cardiac work, hypothermia per se does not cause myocardial ischemia. However, even mild hypothermia decreases tissue damage in response to experimental cardiac ischemia.[93]
Hypothermia decreases blood flow to the kidneys by increasing renal vascular resistance. Inhibition of tubular absorption maintains normal urinary volume. As temperature decreases, reabsorption of sodium and potassium is progressively inhibited, and an antidiuretic hormone-mediated "cold diuresis" results. Despite increased excretion of these ions, plasma electrolyte concentrations usually remain normal. Kidney function returns to normal when patients are rewarmed. Respiratory strength is diminished at core temperatures less than 33°C, but the ventilatory CO2 response is minimally affected. Hepatic blood flow and function also decrease, which significantly inhibits the metabolism of some drugs.
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