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Relevant bibliographies by topics / Hyperkalaemia

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Academic literature on the topic 'Hyperkalaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Hyperkalaemia"

1

Cornes, Michael P., Clare Ford, and Rousseau Gama. "Spurious hyperkalaemia due to EDTA contamination: common and not always easy to identify." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 45, no. 6 (September 9, 2008): 601–3. http://dx.doi.org/10.1258/acb.2008.007241.

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Background To study the detection and prevalence of spurious hyperkalaemia due to potassium ethylenediaminetetra-acetic acid (kEDTA) contamination. Methods In a one-month prospective study, serum EDTA, zinc, calcium, magnesium concentrations and alkaline phosphatase activity were measured in samples with serum potassium ≥6.0 mmol/L. Results Twenty-eight out of 117 hyperkalaemic samples were contaminated with EDTA. Only serum zinc values below the reference range had 100% sensitivity for indicating EDTA contamination, but even at an optimal specificity of 89% at least 12 potentially genuine hyperkalaemic samples would be rejected. Conclusion Spurious hyperkalaemia due to kEDTA contamination is common. Gross kEDTA contamination is obvious by marked unexpected hyperkalaemia, hypocalcaemia, hypomagnesaemia and hypozincaemia. Spurious hyperkalaemia due to low concentrations of kEDTA contamination can only be confidently detected by measurement of serum EDTA.

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McFadzean, Will, Paul Macfarlane, Latifa Khenissi, and Joanna C. Murrell. "Repeated hyperkalaemia during two separate episodes of general anaesthesia in a nine-year-old, female neutered greyhound." Veterinary Record Case Reports 6, no. 3 (September 2018): e000658. http://dx.doi.org/10.1136/vetreccr-2018-000658.

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There is an increasing awareness of the development of hyperkalaemia during anaesthesia in otherwise healthy veterinary patients. In the human literature 63 per cent of in-hospital hyperkalaemic episodes are associated with drug administration. Anecdotal veterinary reports have suggested that a genetic component may also play a role, with greyhounds seemingly more susceptible to the development of hyperkalaemia under anaesthesia. This case report identifies the repeated development of hyperkalaemia, and its treatment, during two separate episodes of general anaesthesia in a nine-year-old, female neutered greyhound. The first episode of hyperkalaemia (7.89 mmol/l) was identified due to bradycardia and second-degree atrioventricular block on electrocardiogram. Treatment was with intravenous calcium gluconate, insulin, glucose and fluid therapy. The second episode (6.60 mmol/l) was associated with spiked T-waves, and treatment was with insulin and glucose infusions to allow completion of the anaesthetic and surgery. Possible causes and treatments are discussed, and the need for reporting of such cases is highlighted.

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McNeill, Holly, and Chris Isles. "Electrocardiographic recognition of life-threatening hyperkalaemia: the hyperkalaemic Brugada sign." JRSM Open 10, no. 9 (September 2019): 205427041983424. http://dx.doi.org/10.1177/2054270419834243.

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Lesson Consider life-threatening hyperkalaemia if the ECG shows high take-off with coved ST segment elevation and negative T wave in lead V1 superimposed on other ECG signs of hyperkalaemia and treat with calcium gluconate while waiting for blood chemistry results.

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Nyirenda, M. J., J. I. Tang, P. L. Padfield, and J. R. Seckl. "Hyperkalaemia." BMJ 339, oct23 1 (October 23, 2009): b4114. http://dx.doi.org/10.1136/bmj.b4114.

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R, Manasa, Aksa Johnson, Presly Thomas Augustine, and Anjana Tom. "Assessment of Predictors of Hyperkalemia in Cardiovascular Diseased Patients." Journal of Drug Delivery and Therapeutics 11, no. 2 (March 15, 2021): 51–54. http://dx.doi.org/10.22270/jddt.v11i2.4587.

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Purpose: The objective is to determine the predictors of hyperkalaemia, severity of hyperkalaemia and to access the prevalence of cardiovascular diseases Methodology: A cross sectional observational study was conducted on the predictors of hyperkalaemia in CVD patients, in a tertiary care teaching hospital for a period of 6 months. Results: Among 105 patients, there were 83 males and 22 females, the age group from 41-60 year shows more CVDs and 61-80 years aged patients are more prone to hyperkalaemia and shows more prevalent when compared to other age groups. The major risk factors of hyperkalaemia were Drugs (30.23%), Disease (58.13%), and Drug interactions (11.62%).Among the cardiovascular diseases, Myocardial Infarction (38%) were the most common type of CVD, while in hyperkalaemia Ischemic Heart Disease (48.83%) were more prevalent. The severity of hyperkalaemia is measured as Mild (60.46%), Moderate (37.20%), and Severe (2.32%). Conclusion: The present study was carried out in order to assess the predictors, prevalence and severity of hyperkalaemia in cardiovascular disease patients. Our study concluded that patients with cardiovascular disease can have an increased risk of hyperkalaemia. Keywords: CVD, Hyperkalaemia, Cross sectional observational study, Predictors, Prevalence, Severity.

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Gross, P., and F. Pistrosch. "Hyperkalaemia: again." Nephrology Dialysis Transplantation 19, no. 9 (August 6, 2004): 2163–66. http://dx.doi.org/10.1093/ndt/gfh284.

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Cheng, C. J., C. S. Lin, L. W. Chang, and S. H. Lin. "Perplexing hyperkalaemia." Nephrology Dialysis Transplantation 21, no. 11 (September 12, 2006): 3320–23. http://dx.doi.org/10.1093/ndt/gfl389.

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Lexchin, Joel. "Treating hyperkalaemia." Lancet 361, no. 9357 (February 2003): 616. http://dx.doi.org/10.1016/s0140-6736(03)12544-5.

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Hoye, Angela, and Andrew Clark. "Iatrogenic hyperkalaemia." Lancet 361, no. 9375 (June 2003): 2124. http://dx.doi.org/10.1016/s0140-6736(03)13724-5.

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Taylor, Polly, Caroline Prymak, John Hird, Sophie Adamantos, Paul MacFarlane, and Will McFadzean. "Unanticipated hyperkalaemia." Veterinary Record 182, no. 3 (January 19, 2018): 84.2–84. http://dx.doi.org/10.1136/vr.k206.

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Dissertations / Theses on the topic "Hyperkalaemia"

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Leitch, Stewart Paul. "Interactive effects of potassium, acidosis, catecholamines and calcium on the heart." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240648.

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Cope, Richard Adrian. "An experimental investigation into the early treatment of life threatening hyperkalaemia." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307574.

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Abensur, Laure. "Dyskaliémie : fréquence, pronostic, prise en charge et iatrogénèse Hypokalemia is frequent and has prognostic implications in stable patients attending the emergency department Hyperkalaemia and hypokalaemia outpatient management: a survey of 500 French general practitioners Dyskalemia: a management problem for students." Thesis, Université de Lorraine, 2020. http://www.theses.fr/2020LORR0200.

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Contexte. Les troubles du potassium sont fréquents et associés à une augmentation de la mortalité toutes causes confondues, prenant la forme d’une courbe en U. Néanmoins, il existe peu de données sur les dyskaliémies en service d’urgence, en particulier chez des patients non critiques, alors qu’ils représentent une part importante de l’activité des services d’urgence. De plus, nous n’avons pas de données concernant les prises en charge des dyskaliémies par les médecins généralistes. Objectifs : Les objectifs étaient d’étudier les facteurs associés à une dyskaliémie chez des patients non critiques aux urgences, et, de connaître les pratiques des médecins généralistes et des internes de médecine générale face à la découverte d’une hyper ou d’une hypokaliémie (seuils connus, seuils de prise en charge et attitude face aux médicaments ayant une action sur la kaliémie). Méthodes. Pour le premier article, nous avons utilisé les données d’une étude observationnelle transversale multicentrique (onze centres d’urgences). Pour le second article, nous avons mené une enquête téléphonique auprès de 500 médecins généralistes répartis sur le territoire français. Pour le troisième article, nous avons interrogé 357 internes en médecine générale à l’aide d’auto-questionnaires. Résultats. Nous avons décrit les facteurs associés à la présence d’une dyskaliémie dans les services d’urgences chez des patients se présentant dans un état médical non critique. La dyskaliémie y est fréquente et l’hypokaliémie retrouvée chez près de 50 % des patients. Cette proportion est plus importante que celle décrite dans des populations comprenant l’ensemble des passages aux urgences, suggérant que l’hypokaliémie serait prépondérante chez des malades non critiques. L’hypokaliémie est dans cette population associée au sexe féminin et à l’usage des diurétiques thiazidiques. Elle est également associée à un pronostic plus défavorable. En ce qui concerne l’hyperkaliémie, elle était associée aux médicaments bloqueurs du système rénine angiotensine aldostérone et à l’insuffisance rénale chronique. Notre enquête auprès de 500 médecins généralistes du territoire français montre qu’il existe une grande hétérogénéité de la prise en charge des dyskaliémies par les médecins généralistes et que certaines pratiques ne sont pas optimales, par exemple le non contrôle biologique en cas d’hyperkaliémie ou encore l’arrêt définitif de médicaments ayant un effet de protection cardio-vasculo-rénale démontrée. Notre enquête auprès des internes a révélé une grande similitude de pratiques avec celle des médecins en exercice. En effet, que ce soit chez les médecins généralistes ou les internes, les seuils usuels de dyskaliémies sont connus et les divergences reflètent bien les différentes définitions retrouvées dans la littérature. Le résultat le plus saillant est le fait que l’hypokaliémie semble plus négligée que l’hyperkaliémie. Conclusions. Nos trois études convergent vers une probable méconnaissance du risque de gravité de l’hypokaliémie. L’ensemble de ces données confirme l’hypothèse d’une gestion sous-optimale des dyskaliémies, et principalement de l’hypokaliémie en médecine de ville, contribuant possiblement à sa prépondérance aux urgences, pour les patients non critiques. L’hypokaliémie représente une tueuse silencieuse et méconnue qu’il conviendrait de démasquer et de faire mieux connaître, pour un potentiel impact en terme de santé publique
Context: Potassium disorders are frequent and associated with increased all-cause mortality, taking the form of a U-shaped curve. Nevertheless, there are little data on dyskalemia in the emergency department, especially in non-critical patients, even though it represents a significant part of the activity of emergency departments. Moreover, we have no data on the management of dyskalemia by general practitioners. Objectives: The objectives were to study the factors associated with dyskalemia in non-critical patients in the emergency department, and to learn about the practices of general practitioners and residents faced with the discovery of hyper or hypokalemia (known thresholds, management thresholds and attitude towards drugs with an action on kalemia). Methods: For the first article, we used data from a multi-center (11 emergency centers) cross-sectional observational study. For the second article, we conducted a telephone survey of 500 general practitioners throughout France. For the third article, we interviewed 357 general practice residents using self-administered questionnaires. Results: We described the factors associated with the presence of dyskalemia in emergency departments in patients presenting with non-critical medical condition. Dyskalemia is common and hypokalemia was found in almost 50% of patients. This proportion is higher than that described in populations with all emergency department visits, suggesting that hypokalemia is prevalent in non-critical patients. Hypokalemia in this population is associated with female gender and the use of thiazide diuretics. It is also associated with a poorer prognosis. Hyperkalemia was associated with angiotensin-aldosterone renin system blocker drugs and chronic renal failure. Our survey of 500 general practitioners in France shows that there is great heterogeneity in the management of dyskalemia by general practitioners and that some practices are not optimal, for example the non-biological control in case of hyperkalemia or the definitive discontinuation of proven cardiovascular-renal protection drugs. Our survey of residents revealed a great similarity of practices with those of practicing physicians. In fact, both in general practitioners and residents, the usual thresholds for dyskalemia are known and the differences reflect the different definitions found in the literature. The most salient result is the fact that hypokalemia seems to be more neglected than hyperkalemia. Conclusions: Our three studies converge on the basis that the risk of hypokalemia severity is probably not well known. All these data confirm the hypothesis that a sub-optimal management of dyskalemia, and mainly hypokalemia in primary care, may contribute to its preponderance in emergency rooms, for non-critical patients. Hypokalemia has a potential negative impact in terms of public health as it represents a silent and little-known killer that should be unmasked and exposed

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Siew, Keith. "Gitelman & Gordon : mirror image syndromes reveal the roles of WNKs in blood pressure homeostasis and novel anti-hypertensive targets." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289398.

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Study of Gordon (PHAII) and Gitelman (GS) syndromes revealed the importance of the WNK pathway and thiazide-sensitive Na-Cl Cotransporter (NCC) in the renal control of blood pressure. PHAII mutations lead to WNK accumulation resulting in the hyperphosphorylation of the downstream effector, SPAK, which overactivates NCC causing salt retention and hypertension. Mutations causing deletion of exon-9 in Cullin-3, which normally ubiquitylates WNKs for degradation, were recently discovered to cause the severest subtype of PHAII (PHA2E) with early onset salt-sensitive hypertension and hyperkalaemia. The reasons for this severity have remained elusive, however clues came from SPAK knock-out mice which recapitulate GS, the phenotypic mirror image of PHAII, typically caused by activation-inhibiting NCC phosphorylation site mutations resulting in salt-wasting and hypotension. As these mice were also discovered to have reduced vascular tone, it suggests the WNK pathway may have extra-renal roles in vascular smooth muscle function and highlights inhibition of SPAK function as a promising anti-hypertensive strategy with multiple sites of action. To address these possibilities the work aimed to phenotype: (1) heterozygous CUL3$^{WT/\Delta403-459}$ mice to investigate a possible vascular contribution to PHAII pathophysiology, (2) homozygous knock-out mice of MO25, a master regulator known to increase SPAK activity up to 100-fold independent of WNKs, and (3) homozygous SPAK$^{L502A/L502A}$ knock-ins, predicted to have disrupted SPAK binding to WNK/NCC, in order to validate SPAK signalling inhibition as a viable anti-hypertensive strategy. In mice, the CUL3$^{\Delta403-459}$ proteins are hyperflexible, hypermodified and ultimately have reduced WNK ubiquitylation. This lead to hypertension, hyperkalaemia, hyperchloraemia with compensated metabolic acidosis and growth retardation, which closely recapitulates human PHA2E. The discovery of increased vascular tone suggests an explanation for the severity of CUL3$^{\Delta}$$^{ex9}$PHAII. In mice, homozygous MO25$\alpha$ knock-out proved embryonically lethal, while homozygous MO25$\beta$ knock-out did not meaningfully alter blood pressure or electrolyte homeostasis. However, the SPAK$^{L502A}$ protein had a decreased ability to bind WNKs and cation-chloride cotransporters NCC and NKCC1/2, serving to reduce their activation. SPAK$^{L502A/L502A}$ mice showed typical features of GS with mild hypokalaemia, hypomagnesaemia, hypocalciuria and salt-wasting hypotension. The mice also presented with decreased markers of vascular tone potentially due to effects on cardiovascular and neuronal NKCC1. These results show that SPAK binding is crucial for blood pressure control and pharmacological inhibition of this binding is an attractive anti-hypertensive strategy.

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Books on the topic "Hyperkalaemia"

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Wingo, Charles S., and I. David Weiner. Approach to the patient with hypo-/hyperkalaemia. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0034_update_001.

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The differential diagnosis and approach to patients with high or low serum potassium are described. Patients with either abnormality have an increased mortality in large population-based studies. Most have significant renal, cardiovascular, endocrine, liver, or gastrointestinal disease. They are frequently taking prescription or other drugs and the evaluation of their electrolyte disorder should not be conducted in isolation, but within the context of their disease or diseases. The presence of isolated hypokalaemia or hyperkalaemia in the absence of these other diseases or any apparent drug administration should prompt the clinician to re-consider the clinical history and the reported laboratory values.

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Stacey, Victoria. Renal emergencies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199592777.003.0012.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Biochemical crises. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0036.

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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma potassium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0173.

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Potassium is the major intracellular cation, and maintenance of potassium homeostasis is critical for normal cellular function. Serum potassium levels usually range from 3.5–4.5 mmol/l (compared with intracellular levels of ~150 mmol/l). Hypokalaemia is defined as a serum potassium level <3.5 mmol/l, and hyperkalaemia as a serum potassium level >4.5 mmol/l. Hyperkalaemia occurs in over 5% of hospitalized patients, and is most common in older age groups, where it is associated with renal impairment and medication use. Medications that block the renin–angiotensin system, such as angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers, are often responsible. Hypokalaemia is also common, affecting over 15% of hospitalized patients, and is usually related to diuretic use, gastrointestinal losses, or inadequate potassium in the diet. This chapter reviews the causes and management of derangements of plasma potassium.

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Frise, Matthew C., and Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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Fox, Grenville, Nicholas Hoque, and Timothy Watts. Fluids and electrolytes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198703952.003.0005.

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This chapter provides an overview of the background of fluid balance in the neonate, including the need to compensate for fluid loss (output), and the requirement to provide energy and nutrition. It also covers the management of common issues in fluid, electrolyte, and acid-base balance in the newborn period, including dehydration, sodium balance (hyponatraemia and hypernatraemia), hyperkalaemia, interpretation of blood gases (including pH, base excess, and anion gap), respiratory and metabolic acidosis, and hydrops fetalis.

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Jörres, Achim, Dietrich Hasper, and Michael Oppert. Electrolyte and acid–base disorders in AKI. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0230.

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Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of underlying problems and physiological compensatory mechanisms. In metabolic acidosis, a bicarbonate deficit may be corrected by sodium bicarbonate administration. Of note, whilst patients with AKI tend to retain electrolytes such as potassium and phosphate, this might be reversed during renal replacement therapy and even substitution of these losses may be required.

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Lavalle, Carlo, Renato Pietro Ricci, and Massimo Santini. Conduction disturbances and pacemaker. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0055.

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The most frequent clinical conditions complicated by bradyarrhythmias or atrioventricular blocks seen in an emergency setting are the degeneration of the conduction system, acute myocardial infarction, drug toxicity, and hyperkalaemia. Pacemaker malfunction is another cause of potentially life-threatening bradyarrhythmias. The presence of signs/symptoms of hypoperfusion and the localization of the block condition the therapeutic approach. Treatment of bradyarrhythmias and atrioventricular block in a critical care setting may be preventative or therapeutic. A preventative approach is necessary when the risk of a sudden block with an inadequate ventricular escape rhythm is present, but the patient is asymptomatic. Symptomatic patients require immediate treatment. If the block is located at His bundle level or at bundle branch level, atropine may be ineffective and may even worsen the degree of the block. If drug administration is ineffective, transvenous temporary pacing is indicated. Transcutaneous cardiac pacing is another temporary method of pacing indicated in various critical clinical settings.

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Lapostolle, Frédéric, and Stephen W. Borron. Management of digoxin poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0323.

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Despite a gradual decline in the clinical use of digitalis glycosides, digitalis toxicity continues to be responsible for substantial morbidity and mortality, particularly among the elderly. Digitalis poisoning may occur acutely, after intentional overdose, but is more often seen as the result of chronic intoxication among patients receiving digitalis therapy. Clinical findings in chronic digitalis poisoning are often subtle. The astute clinician will enquire about digitalis use in older patients with vague complaints and will not be dissuaded from considering digitalis toxicity in the face of a ‘therapeutic’ digitalis blood concentration. Two digitalis preparations continue to be used with frequency, depending on geography. Digoxin is the digitalis glycoside of choice in the USA, while digitoxin prevails in some parts of Europe. While the methods and half-lives of elimination differ markedly for these two substances, the approach to poisoning by either is similar. Advanced age, underlying cardiovascular disease, and severe hyperkalaemia represent poor prognostic factors in digitalis poisoning. Early administration of digitalis Fab fragments should be undertaken when life-threatening symptoms are present. Prophylactic therapy with reduced doses of Fab fragments should be strongly considered for less serious toxicity.

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Book chapters on the topic "Hyperkalaemia"

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Woerlee, G. M. "Hyperkalaemia." In Common Perioperative Problems and the Anaesthetist, 442–49. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1323-3_75.

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Findlay, Mark, and Christopher Isles. "Hyperkalaemia." In Clinical Companion in Nephrology, 89–94. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14868-7_18.

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"Hyperkalaemia." In Differential Diagnosis in Small Animal Medicine, 437. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470751190.ch64.

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Gonem, Sherif. "Hyperkalaemia." In Diagnosis in Acute Medicine, 150–51. CRC Press, 2017. http://dx.doi.org/10.4324/9781315383798-37.

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Mahadevan, V., and Anil Asokan. "Hyperkalaemia." In Postgraduate Topics in Anaesthesia, 148. Jaypee Brothers Medical Publishers (P) Ltd., 2011. http://dx.doi.org/10.5005/jp/books/11286_47.

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Crook, Martin. "Hyperkalaemia." In Case Presentations in Chemical Pathology, 1–4. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-7506-0845-9.50007-4.

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McMillan, Matt. "Hyperkalaemia – myocardial toxicity." In BSAVA Cognitive Aids for Anaesthesia in Small Animal Practice, 50–51. British Small Animal Veterinary Association, 2020. http://dx.doi.org/10.22233/9781910443910.30.

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Mehta, Arjun. "Chapter-14 Hyperkalaemia." In Emergency Medicine, 34–35. Jaypee Brothers Medical Publishers (P) Ltd., 2005. http://dx.doi.org/10.5005/jp/books/10253_15.

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Firth, John D. "Disorders of potassium homeostasis." In Oxford Textbook of Medicine, edited by John D. Firth, 4748–63. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0474.

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Abstract:

Hypokalaemia is defined as a serum potassium concentration lower than 3.5 mmol/litre and is the most common electrolyte abnormality seen in clinical practice, found in about 20% of hospital inpatients. Clinical features and investigation—mild hypokalaemia is asymptomatic, but nonspecific symptoms develop with more severe disturbance, and serious neuromuscular problems sometimes arise at serum potassium concentrations lower than 2.5 mmol/litre. Emergency management is rarely required, but intravenous infusion of potassium should be given in the rare circumstances of life-threatening cardiac arrhythmia or muscular paralysis. There are a very large number of possible causes of hypokalaemia, the most common causes being diuretics (particularly thiazides), vomiting, and diarrhoea. The most common genetic cause is Gitelman’s syndrome. Management is with potassium and magnesium supplements. Other causes of tubular wasting of potassium include Bartter’s syndrome and mineralocorticoid excess. There are several rare conditions in which hypokalaemia is associated with episodes of extreme weakness/paralysis, including thyrotoxic periodic paralysis and familial hypokalaemic periodic paralysis. Hyperkalaemia, defined as a serum potassium concentration of greater than 5.0 mmol/litre, is asymptomatic, and severe hyperkalaemia (>7 mmol/litre) is the most serious of all electrolyte disorders because it can cause cardiac arrest. The electrocardiogram (ECG) is the best guide to the significance of hyperkalaemia in any particular individual. Patients with ECG manifestations more severe than tenting of the T waves should be given intravenous calcium gluconate (10 ml of 10%) followed by intravenous insulin and glucose, or nebulized salbutamol. There are many causes of hyperkalaemia, but by far the most common are renal failure and/or drugs. Other causes include exhaustive exercise, acidosis, drugs, and hyperkalaemic periodic paralysis (very rare).

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Stewart, Andrew. "The patient with hyperkalaemia." In Pocket On Call, edited by Rory Mackinnon, 74–79. CRC Press, 2015. http://dx.doi.org/10.1201/b18026-16.

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Conference papers on the topic "Hyperkalaemia"

1

Monasterio, Violeta, Jesus Carro, Esther Pueyo, and Jose F. Rodriguez. "The role of purkinje automaticity as an arrhythmia mechanism in hyperkalaemia." In 2015 Computing in Cardiology Conference (CinC). IEEE, 2015. http://dx.doi.org/10.1109/cic.2015.7411050.

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2

Liu, Jiaqi, Yuan Gao, Yinglan Gong, Ling Xia, Wenlong Xu, Mingfeng Jiang, and Gangmin Ning. "One-dimensional Simulation of Alternating Conduction under Hyperkalaemic Conditions." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.312-025.

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