FIG. 186-1. Rhythm strip from patient with temperature of 25°C (77°F) showing atrial fibrillation with a slow ventricular response, muscle tremor artifact, and Osborn
Patients are at risk for dysrhythmias at body temperatures below 30°C (86°F); the risk increases as body temperature decreases. Although various dysrhythmias may occur at any time, the typical sequence is a progression from sinus bradycardia to atrial fibrillation with a slow ventricular response, to ventricular fibrillation, and ultimately, to asystole. The hypothermic myocardium is extremely irritable, and ventricular fibrillation may be induced by a variety of manipulations and interventions that stimulate the heart, including rough handling of the patient.46
Pulmonary effects include initial tachypnea, followed by a progressive decrease in respiratory rate and tidal volume. Cold-induced bronchorrhea, along with a depression of cough and gag reflexes, makes aspiration pneumonia a common complication.
Much attention has been paid to the temperature correction of arterial blood gases in the hypothermic patient. Since the blood gas analyzer warms the blood to 37°C (98.6°F), thus increasing the partial pressure of dissolved gases, the machine will report a higher P o2 and Pco2 and lower pH than the actual values at the patient's body temperature. Correction factors and nomograms are available to determine the actual values in the patient's body; however, the optimal or "normal" values in hypothermia are not known. The simplest solution is to use the uncorrected values as if the patient were normothermic; studies suggest that this approach is the most physiologically sound.78 Pco2 is often quite low secondary to depressed metabolism and decreased CO2 production, and iatrogenic hyperventilation may lead to marked respiratory alkalosis.
Hypothermia causes a leftward shift of the oxyhemoglobin dissociation curve, potentially impairing oxygen release to tissues. Patients may have minimal oxygen reserves despite diminished oxygen requirements, warranting the administration of supplemental oxygen.
The CNS is affected by hypothermia, with a progressive depression of consciousness with decreasing temperature. Mild incoordination is followed by confusion, lethargy, and coma; pupils may be dilated and unreactive. These changes are associated with a decrease in cerebral blood flow. An even greater decrease in cerebral oxygen requirements may protect the brain against anoxic or ischemic damage.
Hypothermia impairs renal concentrating abilities and induces a "cold diuresis," leading to significant volume losses. Because of this concentrating defect, urine flow and specific gravity are unreliable indicators of intravascular volume and circulatory status. The immobile hypothermic patient is prone to rhabdomyolysis, and acute tubular necrosis may occur because of myoglobinuria and renal hypoperfusion.
Intravascular volume is also lost due to a plasma shift to the extravascular space. The combination of hemoconcentration, cold-induced increase in blood viscosity, and poor circulation may lead to intravascular thrombosis and subsequent embolic complications. Disseminated intravascular coagulation may occur because of release of tissue thromboplastins into the bloodstream, especially when circulation is restored during rewarming.
Because cold inhibits both platelet function and the enzymatic reactions of the coagulation cascade, hypothermic patients are prone to bleeding. The coagulopathy may be evident clinically but not detected with routine coagulation tests, which are performed at 37°C (98.6°F).
Endocrine function is fairly well preserved at low body temperatures. Plasma cortisol and thyroid hormone levels are usually normal or elevated unless the patient has a preexisting deficiency. Glucose levels may be normal, low, or elevated. Though hyperglycemia is common due to decreased insulin release as well as decreased glucose utilization, hypoglycemia may occur in up to 40 percent of patients.9
Acid-base disturbances are common in hypothermia but follow no uniform pattern. Acidosis may occur due to severe respiratory depression and CO 2 retention and to lactic acid production from shivering and poor tissue perfusion. Alkalosis may result from diminished CO 2 production with low metabolic rates or from iatrogenic hyperventilation or sodium bicarbonate administration.
Pancreatitis (not only hyperamylasemia but true pancreatic necrosis) may occur in hypothermia. Hepatic function is depressed by cold, so drugs normally metabolized, conjugated, or detoxified by the liver (e.g., lidocaine) may rapidly accumulate to toxic levels.
Finally, local cold injury and frostbite may occur in the hypothermic patient. DIAGNOSIS
The diagnosis of hypothermia is often not obvious; exposure to profound cold is not necessary to produce hypothermia. Since many standard clinical thermometers record only to 34.4°C (94°F), low-reading glass or electronic thermometers are required to accurately measure the temperature of hypothermic patients. Electronic thermometers with flexible probes can be used to continuously monitor rectal or esophageal temperatures.
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