PubMed · 27907
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G Habel. 1978-06-15. [Acid-base equilibrium].. https://pubmed.ncbi.nlm.nih.gov/27907/
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BACKGROUND: Adrenaline is used increasingly in the management of septic shock, but its efficacy and safety are uncertain. METHODS: In an open, randomised, crossover study we compared the effects of stepped doses of adrenaline 0.1 to 0.5 microgram/kg per min and dopamine 2.5 to 10 micrograms/kg per min on the haemodynamic and acid-base status of 23 patients critically ill with severe sepsis (n = 10) or severe malaria (n = 13). FINDINGS: All patients completed the dopamine study whereas in 16 (84%) patients the adrenaline infusion had to be terminated before reaching, or during, the maximum dose because of lactic acidosis (p < 0.0002). Adrenaline was associated with a mean (95% CI) increase in plasma lactate of 3.2 (2.6 to 3.8) mmol/L, and mean falls in arterial pH of 0.052 (0.035-0.068) pH units and base excess of 3.8 (2.8-4.7) mmol/L. The geometric mean (95% CI) lactate increment per unit adrenaline dose was 8.2 (5.8-10.5) mmol/L per microgram/kg per min. In contrast dopamine was associated with a fall in lactate of 1.0 (0.4-1.5) mmol/L, a rise in base excess of 1.4 (0.7 to 2.0) mmol/L (p < 0.0001 in each case), and no effect on arterial pH. Both drugs induced significant increases in cardiac index and oxygen delivery with smaller increases in oxygen consumption and falls in systemic vascular resistance which were similar in severe malaria and severe sepsis (p > 0.1 in each case) [corrected]. INTERPRETATION: Infusion of inotropic doses of adrenaline in severe infections causes lactic acidosis.
The effects of glucocorticoids (GC) on the blood-to-tumour barrier transport (BTT) and tissue blood volume (Vb) and aspects of brain tumour acid/base balance were studied in patients with brain tumours using positron emission tomography (PET). BTT was assessed by 82Rb/PET and quantitated as K1 (unidirectional transport constant), tissue blood volume was also measured by 82Rb/PET. The parameters were evaluated following start of GC. The pH was assessed with 11C-DMO/PET as a single measurement in patients receiving GC. GC treatment reduced the tumour K1 20% to 30%, within 6 to 24 hours following start of treatment. Brain tumours were in the alkalotic range compared to normal brain. The studies have helped to explain GC's antioedema effect and mechanisms behind the observed tumor alkalosis. The 82Rb/PET model seems useful for quantitative measurements of such parameters as pharmacological blood-tumour barrier opening, allowing continuous assessment of the potential for tumour chemotherapeutic uptake, thereby improving anti-cancer chemotherapy.
OBJECTIVE: To characterize respiratory function and treatment in dogs with findings compatible with those of human adult respiratory distress syndrome (ARDS) and to evaluate the application in dogs of clinical for diagnosis of ARDS. DESIGN: Retrospective review of medical records. ANIMALS: 19 dogs with acute respiratory distress syndrome. RESULTS: Arterial blood pH was 7.30 +/- 0.59 (mean +/- SD). Nine dogs had metabolic acidosis. In nonmechanically ventilated dogs, PaCO2 was 15.0 to 54.9 mm of Hg. Respiratory acidosis developed in 2 mechanically ventilated dogs. Hypoxemia was observed in 4 of 5 dogs breathing room air. In 4 mechanically ventilated dogs, oxygenation was inadequate, despite use of > 60% inspired O2 and positive end-expiratory pressure in 3 dogs. Alveolar-to-arterial oxygen tension gradients were widened in 4 dogs breathing room air and in 6 dogs ventilated with 100% O2. Ten dogs were mechanically ventilated; ventilatory rate was 18 to 60 breaths/min. Tidal volume was 12 +/- 3.8 ml/kg of body weight in 4 dogs, minute ventilation > 400 ml/kg/min in 2 dogs, and peak airway pressures > 25 cm of H2O in 6 dogs. Positive end-expiratory pressure was used in 8 dogs. Pneumothorax was detected in 5 ventilated dogs. Human clinical criteria for diagnosis of ARDS were fulfilled in 7 dogs. Fluid treatment consisted of IV crystalloids and synthetic colloids. Drugs most often administered were antibiotics and loop diuretics. CLINICAL IMPLICATIONS: Human clinical criteria for identification of ARDS may be helpful in diagnosis of acute respiratory distress syndrome in dogs.