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PubMed1987

Blood gas studies in dogs with severe steam inhalation injury.

The dynamic changes in blood gases in 34 dogs suffering severe steam inhalation injury were studied during the first 14 days post-burn to determine the effects of inhalation injury on lung function. Nineteen dogs received only severe steam inhalation injury, while 15 other dogs received both 30 per cent total body surface area (TBSA) deep burns and steam inhalation injury. The results showed marked reductions of PaO2, PaCO2, AB, SBE, T-CO2, SB, BBp, pHNR and SatO2 (P less than 0.05 approximately 0.01), whereas the P(A-a)O2 increased (P less than 0.05 approximately 0.01) within week 1 post-burn in both groups. These data suggest that the injured animals were suffering from hypoxaemia and respiratory alkalosis induced by disturbance of the gas-exchange function of the lungs. There was also metabolic acidosis, which was closely related to high fever, excessive catabolism, and particularly to hypoxaemia in week 1 post-burn. If the animals survived through the critical period (1-7 days post-burn), most of the abnormal gas parameters then gradually returned to the pre-burn levels. It is clear, therefore, that blood gas monitoring in patients with inhalation injury is not only of diagnostic importance but also of prognostic value.

Acidosis, Respiratory↗

PubMed1996

The relation of ventilatory failure to pulmonary, respiratory muscle and central nervous system disturbances in calves with an experimentally produced pneumonia.

To explore the pathophysiology of respiratory failure in an experimental pneumonia, a Pasteurella haemolytica broth culture was injected intratracheally into 12 calves, which were then studied over a period of 10 h. Measurements were made of inspired minute ventilation (VE), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory rate (RR) and tidal volume (VT)], transdiaphragmatic pressure (Pdi), occlusion pressure at the airway opening 100 milliseconds after onset of inspiration (Pawo100ms), arterial blood gas tensions and pH and recorded diaphragmatic electromyogram (EMGdi) and rectal temperature (Tr). On and after the third hour after inoculation, the animals varied in respect of clinical signs, Tr, RR, VE, Pawo100ms/EMGdi, and arterial gases and pH. In benign cases, diminished alertness, laboured respiration and fall of arterial oxygen pressure (PaO2) worsened up to 7 h after inoculation, but then progressively improved, VE being maintained at approximately 150% baseline throughout the study (10 h). Neither arterial carbon dioxide pressure (PaCO2) nor pH was altered. Moderate cases resembled benign cases in respect of laboured respiration, VE, PaO2 and PaCO2; however, pH was at first maintained at preinoculation levels, but declined thereafter. In severe cases, the animals were drowsy between hours 3 and 7, and became comatose between hours 8 and 10; in contrast to both benign and moderate cases: (1) RR was reduced by hour 5, (2) there was no trend towards recovery of PaO2 and pH, (3) VE, Pdi, Pawo100ms and Pawo100ms/EMGdi were severely decreased, and (4) PaCO2 increased. These results suggest that pneumonia does not alter ventilatory neuromuscular pump function in calves, unless concomitant cardiovascular collapse occurs. It is not clear whether fatal ventilatory failure is caused mainly by deterioration in ventilatory muscle fibre processes or structures, altered central nervous system adjustment of ventilatory timing, or cardiovascular dysfunction. However, inspiratory pressures fall when excitation to the diaphragm is still growing, which suggests peripheral respiratory muscle fatigue.

Acidosis, Respiratory↗

PubMed2001

Sensitivity of the spiny dogfish (Squalus acanthias) to waterborne silver exposure.

The physiological effects of waterborne silver exposure (added as AgNO(3)) on spiny dogfish, Squalus acanthias, were evaluated at 30, 200 and 685 microg silver per l in 30 per thousand seawater. These concentrations cover the toxic range observed for freshwater teleosts, where silver is extremely toxic, to seawater teleosts which tolerate higher silver concentrations. However, these levels are considerably higher than those that occur in the normal environment. At 685 microg l(-1), dogfish died within 24 h. Causes of death were respiratory as well as osmoregulatory failure. Arterial P(a)O(2) rapidly declined below 20 Torr, and blood acidosis (both respiratory and metabolic) occurred. Urea excretion increased dramatically and plasma urea dropped from 340 to 225 mM. There were pronounced increases in plasma Na(+), Cl(-), and Mg(2+), indicative of ionoregulatory failure due to increased diffusive permeability as well as inhibited NaCl excretion. At 200 microg l(-1), fish died between 24 and 72 h of silver exposure. The same physiological events occurred with a small time delay. At 30 microg l(-1), effects were much less severe, although slight mortality (12.5%) still occurred. Respiratory alkalosis occurred, together with moderate elevations in plasma Na(+) and Cl(-) levels. Silver accumulated to the highest concentrations on gills, with only low levels in the intestine, in accord with the virtual absence of drinking. Na(+)/K(+)-ATP-ase activities of gill and rectal gland tissue were impaired at the highest silver concentration. Normal gill function was impaired due to swelling and fusion of lamellae, lamellar aneurism and lifting of the lamellar epithelium. Our results clearly indicate that this elasmobranch is much more sensitive (about 10-fold) to silver than marine teleosts, with silver's toxic action exerted on the gill rather than on the intestine, in contrast to the latter.

Animals↗

PubMed1966