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This report describes the historical development in the clinical application of chemical variables for the interpretation of acid-base disturbances. The pH concept was already introduced in 1909. Following World War II, disagreements concerning the definition of acids and bases occurred, and since then two strategies have been competing. Danish scientists in 1923 defined an acid as a substance able to give off a proton at a given pH, and a base as a substance that could bind a proton, whereas the North American Singer-Hasting school in 1948 defined acids as strong non-buffer anions and bases as non-buffer cations. As a consequence of this last definition, electrolyte disturbances were mixed up with real acid-base disorders and the variable, strong ion difference (SID), was introduced as a measure of non-respiratory acid-base disturbances. However, the SID concept is only an empirical approximation. In contrast, the Astrup/Siggaard-Andersen school of scientists, using computer strategies and the Acid-base Chart, has made diagnosis of acid-base disorders possible at a glance on the Chart, when the data are considered in context with the clinical development. Siggaard-Andersen introduced Base Excess (BE) or Standard Base Excess (SBE) in the extracellular fluid volume (ECF), extended to include the red cell volume (eECF), as a measure of metabolic acid-base disturbances and recently replaced it by the term Concentration of Titratable Hydrogen Ion (ctH). These two concepts (SBE and ctH) represent the same concentration difference, but with opposite signs. Three charts modified from the Siggaard-Andersen Acid-Base Chart are presented for use at low, medium and high altitudes of 2500 m, 3500 m, and 4000 m, respectively. In this context, the authors suggest the use of Titratable Hydrogen Ion concentration Difference (THID) in the extended extracellular fluid volume, finding it efficient and better than any other determination of the metabolic component in acid-base disturbances. The essential variable is the hydrogen ion.
The effects of acepromazine-ketamine on the heart rate, arterial blood pressure, respiratory rate, blood gases, arterial blood pH, and temperature were investigated in six healthy sheep. Ketamine (11 mg/kg i.v.) was given 15 min after administration of acepromazine (0.05 mg/kg i.m.) A catheter was placed in the carotid artery for arterial blood sampling and recording of mean arterial blood pressure. All parameters were evaluated before the administration of acepromazine and at 5, 15, 30, 45, and 60 min following the injection of ketamine. The arterial blood pressure was recorded in 30 s after the injection of ketamine as well. The heart rate decreased significantly at minutes 15, 30, 45, and 60. The mean arterial blood pressure declined significantly at 30 s and 45 min. The mean respiratory rate decreased significantly at 45 and 60 min. PaO₂ decreased significantly at 5, 15, and 45 min, and PaCO₂ increased at 5 min. The pH values decreased significantly at 5, 15, and 30 min. The body temperature decreased significantly at all points in time. The data showed that the combination of acepromazine-ketamine caused an inhibition of the cardiovascular system. This combination is responsible for little distributed ventilation, decreased PaO₂, increased PaCO₂, decreased pH values, and a declined in body temperature in the anaesthesia period in sheep.
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