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Respiratory alkalosis acute

In patients with severe exacerbations, monitoring of Pco2 should be considered. Patients with acute asthma usually have a respiratory alkalosis, and a normal or increased Pco2 indicates the potential for respiratory failure. [Pg.229]

Acute respiratory alkalosis t Decreased3 -Normal AHCO3- = 0.2 x ARaCCy... [Pg.421]

H. Kusuoka, P.H. Backx, M.C. Camilion de Hurtado, M. Azan-Backx, E. Marban, H.E. Cingolani, Relative roles of intracellular Ca + and pH in shaping myocardial contractile response to acute respiratory alkalosis. Am. J. Physiol. 265 (1993) HI 696-1703. [Pg.270]

Nausea, vomiting, tinnitus, and hyperventilation are seen early in toxicity. As severity of toxicity increases, intractable vomiting, hyperthermia, hypotension, tachycardia, confusion, coma, seizures, pulmonary edema, acute renal failure, and death may occur. Hyperglycemia may be seen early, whereas hypoglycemia may occur later in toxicity. Acid-base disturbances such as respiratory alkalosis and/or metabolic acidosis may be noted. Signs and symptoms of salicylate toxicity may be noted as blood levels rise over 30mgdN. ... [Pg.37]

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... [Pg.378]

Increased plasma Cl" concentration, Uke increased Na concentration, occurs with dehydration, RTA, acute renal failure, metabohc acidosis associated with prolonged diarrhea and loss of sodium bicarbonate, DI, states of adrenocortical hyperfimction, and overtreatment with saline solutions. A slight rise in Cl" concentration may also be seen in respiratory alkalosis due to the renal compensation of excreting... [Pg.1757]

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. [Pg.996]

The initial response of the body to acute respiratory alkalosis is chemical buffering. Hydrogen ions are released from the body s buffers— intracellular proteins, phosphates, and hemoglobin—and titrates down the serum bicarbonate concentration. This process occurs within minutes. Acutely, the bicarbonate concentration can be decreased by a maximum of 3 mEq/L for each 10-mm Hg decrease in PaC02 (see Table 5IM). When only the physicochemical buffering has occurred, the disturbance is referred to as acute respiratory alkalosis. [Pg.997]

Respiratory alkalosis is much less common than acidosis but can occur when respiration is stimulated or is no longer subjcci to feedback control (Fig. 4). Usually these are acute conditions, and there is no renal compensation. The treatment is to inhibit or remove the cause of the hyperventilation, and the acid-base balance should return to normal. Examples are ... [Pg.103]

Figure 3.4 Identification of various acid-base disturbances. Acute disorders are synonymous with uncompensated disturbances, whereas chronic conditions are synonymous with partially compensated or compensated disturbances. If a specific case falls outside the shaded areas, a compound acid-base disturbance may be suspected, such as the coexistence of respiratory acidosis (partially compensated) and metabolic alkalosis. Unshaded areas may also indicate a transient state between an acute (uncompensated) state and a chronic (partially compensated) condition. (From Cogan MG, Rector FC Jr., Seldin DW. In Brenner BM, and Rector FC Jr, eds. The Kidney, 2nd ed., Vol. 1, Philadelphia WB Saunders, 1986, p. 860.)... Figure 3.4 Identification of various acid-base disturbances. Acute disorders are synonymous with uncompensated disturbances, whereas chronic conditions are synonymous with partially compensated or compensated disturbances. If a specific case falls outside the shaded areas, a compound acid-base disturbance may be suspected, such as the coexistence of respiratory acidosis (partially compensated) and metabolic alkalosis. Unshaded areas may also indicate a transient state between an acute (uncompensated) state and a chronic (partially compensated) condition. (From Cogan MG, Rector FC Jr., Seldin DW. In Brenner BM, and Rector FC Jr, eds. The Kidney, 2nd ed., Vol. 1, Philadelphia WB Saunders, 1986, p. 860.)...
Arieff AI, Kerian A, Massry SG DeLima J. (1976). Intracellular pH of brain alterations in acute respiratory acidosis and alkalosis. Am J Physiol 230, 804-812. [Pg.227]


See other pages where Respiratory alkalosis acute is mentioned: [Pg.157]    [Pg.157]    [Pg.423]    [Pg.220]    [Pg.259]    [Pg.633]    [Pg.2346]    [Pg.2347]    [Pg.1307]    [Pg.986]    [Pg.986]    [Pg.987]    [Pg.997]    [Pg.998]    [Pg.107]    [Pg.323]    [Pg.961]    [Pg.254]    [Pg.111]    [Pg.65]    [Pg.1774]    [Pg.999]    [Pg.5]   
See also in sourсe #XX -- [ Pg.987 , Pg.997 , Pg.998 , Pg.998 , Pg.999 ]




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