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Compensatory Mechanisms in Acid–Base Disorders
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The plasma bicarbonate ion concentration is increased in metabolic alkalosis and decreased in metabolic acidosis. pH control of ventilation is determined by chemoreceptors in the medulla that monitor the pH of brain ECF and by the pH sensed by the carotid body chemoreceptors. In metabolic acidosis, the low plasma bicarbonate concentration and the increase in blood [H+] induce hyperventilation, lowering and restoring the normal ratio. It is estimated that the ventilatory rate increases about twofold for a change in pH of 0.1 pH unit.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Metabolic alkalosis is a metabolic condition in which there is an increased pH in the tissues. This is a result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. Thiazide diuretics inhibit the sodium-chloride transporter in the distal tubule. With diuretics, the increased hydrogen and potassium ion loss can lead to metabolic alkalosis.
Abdomen
Published in A Sahib El-Radhi, James Carroll, Paediatric Symptom Sorter, 2017
A Sahib El-Radhi, James Carroll
Vomiting usually causes metabolic alkalosis. The presence of metabolic acidosis is suggestive of gastroenteritis or an inborn error of metabolism. The latter possibility is high on the list in the presence of metabolic acidosis without diarrhoea.
The role of the clinical laboratory in diagnosing acid–base disorders
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
When respiratory disorders are complicated with metabolic acid–base disorders, they are called mixed respiratory and metabolic disorders. If the secondary response indicates a bicarbonate level higher or lower than expected, an additional metabolic alkalosis or acidosis, respectively, may be present (Table 3). Almost all critically ill patients have mixed acid–base disorders because many disease processes act simultaneously. As an example, a patient with pneumonia and septic shock will often have hyperventilation, but hypoxia, dehydration, renal failure, and gastrointestinal problems may occur concurrently and result in mixed acid–base problems. Important clues are signs of shock, diarrhea, fluid resuscitation with NaCl (0.9%), and renal failure, all suggestive of metabolic acidosis. Metabolic alkalosis should be considered if the patient is vomiting, because dehydration will lead to renin-angiotensin-aldosterone activation with renal excretion of hydrogen and potassium [70].
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
Acidosis can be either metabolic (primary change is in the plasma bicarbonate), respiratory (primary change is in the pCO2) or both. In primary acute metabolic acidosis, in the absence of associated ventilatory problems, one expects a fall in arterial pCO2 of 1 mmHg from 40 for every mmol/l fall in pHCO3− from 25. If the arterial pCO2 is much higher than expected, a coexistent ventilation type of respiratory acidosis is present. In contrast, if the arterial pCO2 is much lower than expected, concomitant respiratory alkalosis is also present. We refer to the paper by Adrogue et al for a more in-depth study of the expected responses to primary acid base disorders [11]. For correct interpretation of the lab data, the clinical picture must always be integrated. For example, the finding of acidemia, a high arterial pCO2 and an elevated pHCO3- does not indicate that chronic respiratory acidosis is present in absence of a clinical chronic pulmonary condition. The more likely diagnosis is metabolic alkalosis with an acute respiratory acidosis.
Flucloxacillin-induced hypokalaemia: a case report
Published in Acta Clinica Belgica, 2018
Penicillin derivates affect the ion transport in the collecting duct by acting as an non-reabsorbable anion, maintaining a transmembranal voltage potential gradient (negative on the luminal side). This increases the driving force for potassium (K+) secretion by the ROMK and BK channels leading to potassium loss [3,4,11]. In addition, the presence of the non-reabsorbable anion may also enhance hydrogen (H+) secretion in the collecting duct leading to mild metabolic alkalosis. Besides, hypokalaemia itself may contribute to the metabolic alkalosis [8,12]. The co-occurrence of severe hypokalaemia and (mild) metabolic alkalosis caused by high dose penicillin derivates has been described in some case reports but not in all [8,12]. Potentially the metabolic alkalosis is only mild in some cases and was not reported or additional mechanisms may contribute to the hypokalaemia.