Rationale: Hypokalemia occurs in up to 20% of hospitalized patients and is associated with increased incidence of ventricular and atrial fibrillation. It is unclear whether these differing types of arrhythmia result from direct and perhaps distinct effects of hypokalemia on cardiomyocytes. Objective: To investigate proarrhythmic mechanisms of hypokalemia in ventricular and atrial myocytes. Methods and Results: Experiments were performed in isolated rat myocytes exposed to simulated hypokalemia conditions (reduction of extracellular [K + ] from 5.0 to 2.7 mmol/L) and supported by mathematical modeling studies. Ventricular cells subjected to hypokalemia exhibited Ca 2+ overload and increased generation of both spontaneous Ca 2+ waves and delayed afterdepolarizations. However, similar Ca 2+ -dependent spontaneous activity during hypokalemia was only observed in a minority of atrial cells that were observed to contain t-tubules. This effect was attributed to close functional pairing of the Na + -K + ATPase and Na + -Ca 2+ exchanger proteins within these structures, as reduction in Na + pump activity locally inhibited Ca 2+ extrusion. Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepolarizations during hypokalemia, associated with Ca 2+ overload. However, early afterdepolarizations also occurred in untubulated atrial cells, despite Ca 2+ quiescence. These phase-3 early afterdepolarizations were rather linked to reactivation of nonequilibrium Na + current, as they were rapidly blocked by tetrodotoxin. Na + current-driven early afterdepolarizations in untubulated atrial cells were enabled by membrane hyperpolarization during hypokalemia and short action potential configurations. Brief action potentials were in turn maintained by ultra-rapid K + current (I Kur ); a current which was found to be absent in tubulated atrial myocytes and ventricular myocytes. Conclusions: Distinct mechanisms underlie hypokalemia-induced arrhythmia in the ventricle and atrium but also vary between atrial myocytes depending on subcellular structure and electrophysiology.

Background Although electrolyte imbalances (EIs) are common in the emergency department (ED), few studies have examined the occurrence of such conditions in an unselected population. Objectives To investigate the frequency of EI among adult patients who present to the ED, with regards to type and severity, and the association with age and sex of the patient, hospital length of stay (LOS), readmission, and mortality. Methods A retrospective cohort study. All patients ≥ 18 years referred for any reason to the ED between January 1, 2010, and December 31, 2015, who had measured blood electrolytes were included. In total, 62 991 visits involving 31 966 patients were registered. Results EIs were mostly mild, and the most common EI was hyponatremia (glucose-corrected) (24.6%). Patients with increasing severity of EI had longer LOS compared with patients with normal electrolyte measurements. Among all admitted patients, there were 12928 (20.5%) readmissions within 30 days from discharge during the study period. Hyponatremia (glucose-corrected) was associated with readmission, with an adjusted odds ratio (OR) of 1.25 (95% CI, 1.18–1.32). Hypomagnesemia and hypocalcemia (albumin-corrected) were also associated with readmission, with ORs of 1.25 (95% CI, 1.07–1.45) and 1.22 (95% CI, 1.02–1.46), respectively. Dysnatremia, dyskalemia, hypercalcemia, hypermagnesemia, and hyperphosphatemia were associated with increased in-hospital mortality, whereas all EIs except hypophosphatemia were associated with increased 30-day and 1-year mortality. Conclusions EIs were common and increasing severity of EIs was associated with longer LOS and increased in-hospital, 30-days and 1-year mortality. EI monitoring is crucial for newly admitted patients, and up-to-date training in EI diagnosis and treatment is essential for ED physicians.

Background Dysnatremias are common electrolyte disturbances with significant morbidity and mortality. In chronic dysnatremias a slow correction rate (<10 mmol/L/24 h) is indicated to avoid neurological complications. In acute dysnatremias (occurring <48 h) a rapid correction rate may be indicated. Most guidelines do not differ between acute and chronic dysnatremias. In this review, we focus on the evidence-based treatment of acute dysnatremias. Methods A literary search in PubMed and Embase. A total of 72 articles containing 79 cases were included, of which 12 cases were excluded due to lack of information. Results Of 67 patients (70% women) with acute dysnatremia, 60 had hypo- and 7 had hypernatremia. All patients with hyper- and 88% with hyponatremia had a rapid correction rate (> 10 mmol/L/24 h). The median time of correction was 1 day in patients with hypo- and 2.5 days in patients with hypernatremia. The mortality was 7% in patients with hypo- and 29% in patients with hypernatremia. Interpretation Severe acute dysnatremias have significant mortality and require immediate treatment. A rapid correction rate may be lifesaving and is not associated with neurological complications. Chronic dysnatremias, on the other hand, are often compensated and thus less severe. In these cases a rapid correction rate may lead to severe cerebral complications. Electronic supplementary material The online version of this article (10.1186/s13049-019-0633-3) contains supplementary material, which is available to authorized users.