[Physiopathology of shock associated with severe burns].
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Biomedical subjects
Publications and source records attributed to N Aikawa.
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The ratio of arterial oxygen tension to inspired oxygen concentration (PaO2/FIO2) as an index of respiratory function was evaluated in 22 patients with body surface area burns of 15--80%. These results indicate that this ratio is limited in its applicability because extrapulmonary factors, such as cardiac output, oxygen consumption, and arterial oxygen content, can affect this index by alterations in the amount of venous desaturation. Useful estimates of intrapulmonary right to left shunt (Qs/Qt) from PaO2/FIO2 were obtained only when arteriovenous oxygen content differences (avDO2) were between 3--5 ml/dl. There were avDO2 values above and below 3--5 ml/dl in at least 35% of the observations. Under these circumstances, PaO2/FIO2 did not correctly reflect changes in Qs/Qt. Blood gases from central venous catheters did not mirror changes in true mixed venous blood and, thus, can lead to erroneous estimations of Qs/Qt. Rational therapy of reduced arterial oxygen saturation requires measurement of both extra- and intrapulmonary factors contributing to arterial desaturation. Measurement of PaO2/FIO2 alone will not estimate these factors.
In vivo injection of isoproterenol(IPR) (4 mg/kg) in normal rats caused fat cell adenylate cyclase to become desensitized to stimulation by IPR in vitro. In contrast, adenylate cyclase from tissues of burn-injured rats (20% body surface, full-thickness scald) remained fully responsive to stimulation by IPR for several days after injury even though catecholamine excretion was elevated more than twofold. Furthermore, fat cell adenylate cyclase from burn-injured animals was not desensitized after acute in vivo IPR injections, whereas adenylate cyclase from the shams did become desensitized after acute IPR injections. To determine whether the apparent resistance to desensitization in burn-injured rats might be an adaptation to the chronic elevation of catecholamines that follows burn injury, two other rat models in which catecholamines are chronically elevated were studied: one was produced by a twice daily schedule or IPR (1 mg/kg) injections for 3 weeks; the other by 3 weeks' cold exposure (0--4 degrees C). As had been observed in burn injury, adenylate cyclase remained fully responsive to IPR in both models, and adenylate cyclase from the cold-acclimated rats was resistant to desensitization by acute injections of IPR. It therefore seems likely that chronic elevations of catecholamines evoke regulatory mechanisms in target cells to circumvent the desensitizationwhich would otherwise occur consequent to acute exposures to catecholamines. In burn injury this may result in an inadvertent adaptation which contributes to hypermetabolism.
The glucose uptake of a perfused, skin-covered preparation of muscle taken from the rat was altered by prior burn injury to the animal. Animals receiving an 8% deep burn to the back 24 hours prior to testing had a glucose uptake (5.9 +/- 0.85 microM/100 gm/min) which was depressed compared with control nonburned preparations (8.4 +/- 0.34 microM/100 gm/min) (P less than 0.025) at low insulin concentration (35 microU/ml). Higher insulin concentrations (160 microU/ml and 16 microU/ml) produced significant increases in the glucose uptake of both the burned and control animals. At the highest insulin level (16 microU/ml), there was no significant difference between burned and control animals. Preparations from animals burned five days prior to study showed a glucose uptake which was not decreased as compared with control animals at the low level of insulin (35 microU/ml) (7.4 +/- 0.62 microM/100 gm/min), but higher levels of insulin (160 microU/ml and 16 microU/ml) failed to produce a significant increase in glucose uptake (8.4 +/- 0.64 microM/100 gm/min and 8.6 +/- 0.92 microM/100 gm/min, respectively). The values differed significantly (P less than 0.05) from control preparation (11.5 +/- 0.54 microM/100 gm/min) at the insulin level of 16 microU/ml. Two different patterns of altered sensitivity to increased insulin concentrations were noted, depending on the stage of injury. The altered metabolic status of peripheral tissues does contribute to the insulin resistance pheonomenon observed after a burn injury.
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Pulmonary artery catheterization was performed in thirty-nine critically burned patients. Hemodynamic changes, induced by thermal injury and its therapy, were measured. Pulmonary wedge pressure was found to be a more reliable indicator of circulating volume, whereas central venous pressure was often misleading. Measurements of both pulmonary hemodynamics and cardiac output were necessary to manage patients requiring high levels of pulmonary end-expiratory pressure (PEEP). These measurements enable one to define optimum PEEP levels which provide maximum oxygen delivery to the tissues. Depressed myocardial function was seen in the early phase of the injury. In this period dopamine administration increased left ventricular stroke work index with minimal changes in filling pressures. The usefulness of dopamine in treating this early myocardial depression deserves further study. Catheter-related complications were minimal when the catheters were used for periods of three days or less.
The treatment of a moderately large burn usually require blood and its products to restore circulating blood volume, achieve metabolic stabilization, and promote wound healing. This case study demonstrates the remarkable metabolic response to injury in a patient refusing blood products administration. Specific management considerations are discussed.
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