Acid–base disturbances
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
A clinical and drug history and physical examination may reveal the cause of the metabolic alkalosis (Fig. 4.9). Useful laboratory investigations in a metabolic alkalosis may include: plasma Na+, K+, Cl−, Mg2 + urea and creatinine,blood gases,spot urine [Cl−] less than 20 mmol/L suggests the saline-responsive form (volume depletion or contraction) of metabolic alkalosis, and more than 20 mmol/L the saline-non-responsive form.
Compensatory Mechanisms in Acid–Base Disorders
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
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.
Acid–base physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
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 PaCO2 and restoring the normal [HCO3]/PaCO2 ratio. It is estimated that the ventilatory rate increases about twofold for a change in pH of 0.1 pH unit.
High anion gap metabolic acidosis induced by cumulation of ketones, L- and D-lactate, 5-oxoproline and acute renal failure
Published in Acta Clinica Belgica, 2018
Laura Heireman, Boris Mahieu, Mark Helbert, Wim Uyttenbroeck, Jan Stroobants, Marian Piqueur
In the case presented here, the patient was chronically treated with fosfomycin antibiotic therapy. It is not known whether this antibiotic is associated with 5-oxoproline intoxication. Moreover, in addition to the HAGMA, decreased ammonia production due to renal failure and diarrhoea may have contributed to the acidosis. In contrast, vomiting may cause a metabolic alkalosis. However, the so-called delta ratio, defined as [(anion gap-12)/(24-bicarbonate serum concentration)], was 1.3, revealing the presence of a pure HAGMA (range 1.0–2.0). Uncontrolled glycaemia resulting in diminished glutathione levels in combination with chronic paracetamol (and fosfomycin) intake, urosepsis and impaired renal function may have played an important role in the induction of 5-oxoproline acidosis in this case.
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.
Pseudohyperaldosteronism due to mumijo consumption during pregnancy: a licorice-like syndrome
Published in Gynecological Endocrinology, 2018
Konstantinos Stavropoulos, Alexandros Sotiriadis, Dimitrios Patoulias, Konstantinos Imprialos, Roxani Dampali, Vasileios Athyros, Konstantinos Dinas
Physical examination was unremarkable, except for symmetric, bilateral lower limb edema. Serum potassium at admission in Obstetrics Department was 2.7 mmol/l, while serum magnesium was 1.72 mg/dl. The rest serum electrolytes values were within normal range. Office blood pressure level was 152/97 mmHg, calculated three consecutive times with the patient in the seated position for 5 min, using a certified automated pressure gauge and an appropriate branch cuff. Air blood gases examination revealed the presence of metabolic alkalosis, with serum bicarbonate level of 29.4 mmol/l and arterial base excess of 5.4 mmol/l. There were no electrocardiographic findings indicative of hypokalemia. Her rest metabolic profile was within normal values.