HYPERKALEMIA in CKD REFERENCES the Steps to Address Hyperkalemia Include Stabilization, Redistribution, and Excretion/Removal of Potassium

Total Page:16

File Type:pdf, Size:1020Kb

HYPERKALEMIA in CKD REFERENCES the Steps to Address Hyperkalemia Include Stabilization, Redistribution, and Excretion/Removal of Potassium TREATMENT OF HYPERKALEMIA IN CKD REFERENCES The steps to address hyperkalemia include stabilization, redistribution, and excretion/removal of potassium. + 1. Tran HA. Extreme hyperkalemia. 11. Inker LA, Astor BC, Fox CH, et al. KDOQI U.S. Best Practices in Managing South Med J. 2005;98:729-732. commentary on the 2012 KDIGO clinical Table 3. 6 practice guideline for the evaluation and Summary of interventions used for acute or chronic treatment of hyperkalemia 2. Gumz ML, Rabinowitz L, Wingo CS. An K HYPERKALEMIA integrated view of potassium homeostasis. management of CKD. Am J Kidney Dis. May Treatment Route of Onset/ Mechanism Comments N Engl J Med. 2015;373:60-72. 2014;63(5):713-735. in Chronic Kidney Disease duration 3. Alvo M, Warnock DG. Hyperkalemia. 12. Mercier K, Smith H, Biederman J. Renin- West J Med. 1984;141:666-671. angiotensin-aldosterone system 6.8 mmol of calcium, corresponding Intravenous (acute) 1-3 min Membrane Does not affect serum potassium level inhibition: overview of the therapeutic 4. Einhorn LM, Zhan M, Hsu VD, et al. The frequency of to 10 ml CaCl (10%)* or 30 ml 30-60 min potential stabilization Effect measured by normalization of electrocardiographic changes use of angiotensin-converting enzyme calcium gluconate (10%) solutions Dose can be repeated if no effects noted hyperkalemia and its significance in chronic kidney inhibitors, angiotensin receptor blockers, Caution advised in patients receiving digoxin disease. Arch Intern Med. 2009;169:1156-1162. mineralocorticoid receptor antagonists, 50-250 ml hypertonic saline (3-5%)** Intravenous (acute) 5-10 min Membrane Efficacy only in hyponatremic patients 5. Jain N, Kotla S, Little BB, et al. Predictors of and direct renin inhibitors. Prim Care. ~2 h potential stabilization hyperkalemia and death in patients with 2014;41:765-778. cardiac and renal disease. Am J Cardiol. 50-100 mmol sodium bicarbonate Intravenous (acute) 5-10 min Redistribution Sodium may worsen pre-existing hypertension and heart failure 13. Vassalotti JA, Centor R, Turner BJ, et al; U.S. 2012;109:1510-1513. or oral (chronic) ~2 h Efficacy questioned for acute treatment of patients on dialysis Kidney Disease Outcomes Quality Initiative 6. Kovesdy CP. Management of hyperkalaemia (KDOQI). A practical approach to detection 10 units of regular insulin Intravenous (acute) 30 min Redistribution Administer with 50 g of glucose intravenously to prevent hypoglycemia in chronic kidney disease. Nat Rev Nephrol. and management of chronic kidney disease 4-6 h 2014;10:653-662. for the primary care clinician [Epub ahead of ß2-receptor agonists: Intravenous or 30 min Redistribution Effect independent of insulin and aldosterone 7. Sarafidis PA, Blacklock R, Wood E, et al. print September 18 2015]. Am J Med. 2015. 10-20 mg aerosol (nebulized) or nebulized (both 2-4 h Caution in patients with known coronary artery disease 0.5mg in 100ml of 5% dextrose in acute) Prevalence and factors associated with 14. Lehnhardt A, Kemper MJ. Pathogenesis, water (intravenous) hyperkalemia in predialysis patients followed in diagnosis, and management of a low-clearance clinic. Clin J Am Soc Nephrol. hyperkalemia. Pediatr Nephrol. March 40 mg furosemide or equivalent Intravenous (acute) Varies Excretion Loop diuretics for acute intervention 2012;7:1234-1241. 2011;26:377-384. dose of other loop diuretic. Higher or oral (chronic) Until diuresis Loop or thiazide diuretics for chronic management; loop diuretic for GFR <40 ml/min/1.73 m2 15 8. Turgut F, Balogun RA, Abdel-Rahman 15. Sarafidis PA, Georgianos PI, Bakris GL. doses may be needed in patients present or May not be effective in patients with reduced GFR EM. Renin-angiotensin-aldosterone system with advanced CKD longer Advances in treatment of hyperkalemia blockade effects on the kidney in the elderly: in chronic kidney disease. Expert Opin Fludrocortisone acetate ≥0.1 mg Oral (chronic) NA Excretion In patients with aldosterone deficiency, large doses might be needed to effectively lower benefits and limitations. Clin J Am Soc Pharmacother. 2015;16:2205-2215. (up to 0.4-1.0 mg daily) potassium levels Nephrol. 2010;5:1330-1339. Sodium retention, edema, and hypertension might occur, and acceleration of kidney and 16. U.S. Food and Drug Administration (FDA). cardiovascular disease 9. Xie X, Liu Y, Perkovic V, et al. Reninangiotensin Kayexalate. http://www.accessdata.fda.gov/ system inhibitors and kidney and drugsatfda_docs/label/2011/011287s023lbl. Cation exchange resins Oral or rectal (either 1-2 h Excretion Cases of intestinal necrosis, which may be fatal, and other serious GI adverse events have cardiovascular outcomes in patients with pdf. Updated December 2010. Accessed Sodium polystyrene sulfonate acute or chronic), �4-6 h been reported16 CKD: a Bayesian Network meta-analysis of December 22 2015. 25-50 g with or without May cause hypokalemia and electrolyte disturbances16 randomized clinical trials [Epub ahead of print sorbitol Cannot be used in medical emergencies16 17. U.S. Food and Drug Administration (FDA). FDA › Hyperkalemia in Chronic Kidney Disease (CKD) 16 November 17 2015]. Am J Kidney Dis. 2015. Caution in patients with heart failure due to sodium load approves new drug to treat hyperkalemia. › Treatment with RAAS Inhibitors (RAASi) in CKD 10. Kidney Disease: Improving Global Outcomes Cation exchange polymer Oral (either acute 7 h Excretion Binds with many other oral medications (in vitro binding studies), separate the dosing of other http://www.fda.gov/NewsEvents/Newsroom/ (KDIGO) CKD Work Group. KDIGO 2012 › Diagnosis and Evaluation of Hyperkalemia Patiromer 8.4, 16.8, or 25.2 g or chronic) ~48 h oral medications by at least 6 hours 17 *** PressAnnouncements/ucm468546.htm. Should not be used as an emergency treatment for life-threatening hyperkalemia because clinical practice guideline for the evaluation Published October 22 2015. Accessed › Treatment of Hyperkalemia in CKD of its delayed onset of action17 and management of chronic kidney disease. November 24 2015. May result in hypokalemia or hypomagnesemia17 Kidney Int Suppls. 2013;3:1-150. Dialysis Hemodialysis Within Removal Effects of dialysis on serum sodium, bicarbonate, calcium and/or magnesium levels can affect results (acute or chronic); minutes For chronic hemodialysis, missed treatments and 2-day interdialytic interval may have a Peritoneal dialysis Until end of negative impact on outcomes. (chronic) dialysis or This publication has been sponsored and longer**** developed in collaboration with Relypsa, Inc. 30 East 33rd Street *CaCl is caustic and could damage peripheral veins. **Limited data available from clinical studies. ***Clinical studies being done to assess the clinical significance of the in vitro interaction. ****Effects can New York, NY 10016 last for an unspecified length of time, depending on ongoing potassium intake or cellular redistribution. Abbreviations: CKD, chronic kidney disease; GFR, glomerular filtration rate; GI, gastrointestinal; NA, not 800.622.9010 applicable. | Adapted with permission from Kovesdy CP. Management of hyperkalaemia in chronic kidney disease. Nat Rev Nephrol, 2014;10:659-662. Copyright 2014 by Macmillan Publishers Limited. www.kidney.org © 2016 National Kidney Foundation, Inc. 02-10-7259_ABG HYPERKALEMIA TREATMENT WITH RAASi DIAGNOSIS AND EVALUATION IN CKD IN CKD OF HYPERKALEMIA The definition of hyperkalemia varies and limits such as >5.5, Studies show that use of ACEIs or ARBs in people with CKD reduces the Hyperkalemia is often asymptomatic, but patients may complain 1 >6.0, or >7.0 mEq/L are used to indicate severity. Repetitive Table 2. Chronic Risk Factors for risk for kidney failure and cardiovascular events, but their use contributes of nonspecific symptoms such as palpitations, nausea, muscle consecutive measures of serum potassium are needed Hyperkalemia in CKD 5, 6, 7, 8 to hyperkalemia.9 The clinical practice guidelines for the use of RAASi in pain, weakness, or paresthesia. Moderate and especially severe to determine if hyperkalemia is sustained or a transient event. CKD are as follows:10, 11 hyperkalemia can lead to cardiotoxicity, which can be fatal. The Many factors affect potassium homeostasis.2 cause of hyperkalemia has to be determined to prevent future episodes. 14 Risk Factor Due To KDIGO Guidelines suggest that an ARB or ACEI be used in diabetic adults with CKD and urine albumin excretion 30-300 mg/24 hours (or equivalent). (2D) Potassium intake Increased dietary potassium intake from Table 1. Acute Versus Chronic Hyperkalemia 3, 4 salt substitute, potassium-rich heart-healthy KDIGO Guidelines recommend that an ARB or ACEI be used in Emergency diagnostic Elective/etiologic diets, and herbal supplements both diabetic and nondiabetic adults with CKD and urine albumin workup:14 workup:14 Acute Hyperkalemia Chronic Hyperkalemia Metabolic acidosis Potassium shift from the intracellular to the excretion >300 mg/24 hours (or equivalent). (1B) extracellular space 1. Assessment of cardiac function, 1. Comprehensive laboratory workup There is insufficient evidence to recommend combining an kidneys, and urinary tract Caused by abnormal net release of Caused by impairment of RAASi Treatment with ACEIs and ARBs block the ACEI with ARBs to prevent progression of CKD. (Not Graded) 2. Review of medication used potassium from cells, often due to potassium excretory process renin-angiotensin system and cause lower 2. Assessment of hydration status trauma, metabolic acidosis (depends and/or increased potassium load
Recommended publications
  • 1 Fluid and Elect. Disorders of Serum Sodium Concentration
    DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol.
    [Show full text]
  • Study Guide Medical Terminology by Thea Liza Batan About the Author
    Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails ­proficiency­in­communicating­with­healthcare­professionals­such­as­physicians,­nurses,­ or dentists.
    [Show full text]
  • Hyperkalemia Masked by Pseudo-Stemi Infarct Pattern and Cardiac Arrest Shareez Peerbhai1 , Luke Masha2, Adrian Dasilva-Deabreu1 and Abhijeet Dhoble1,2*
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 International Journal of DOI 10.1186/s12245-017-0132-0 Emergency Medicine CASEREPORT Open Access Hyperkalemia masked by pseudo-stemi infarct pattern and cardiac arrest Shareez Peerbhai1 , Luke Masha2, Adrian DaSilva-DeAbreu1 and Abhijeet Dhoble1,2* Abstract Background: Hyperkalemia is a common electrolyte abnormality and has well-recognized early electrocardiographic manifestations including PR prolongation and symmetric T wave peaking. With severe increase in serum potassium, dysrhythmias and atrioventricular and bundle branch blocks can be seen on electrocardiogram. Although cardiac arrest is a worrisome consequence of untreated hyperkalemia, rarely does hyperkalemia electrocardiographically manifest as acute ischemia. Case presentation: We present a case of acute renal failure complicated by malignant hyperkalemia and eventual ventricular fibrillation cardiac arrest. Recognition of this disorder was delayed secondary to an initial ECG pattern suggesting an acute ST segment elevation myocardial infarction (STEMI). Emergent coronary angiography performed showed no evidence of coronary artery disease. Conclusions: Pseudo-STEMI patterns are rarely seen in association with acute hyperkalemia and are most commonly described with patient without acute cardiac symptomatology. This is the first such case presenting concurrently with cardiac arrest. A brief review of this rare pseudo-infarct pattern is also given. Keywords: Cardiac arrest, Hyperkalemia, Myocardial infarction, STEMI, ECG Background Case presentation Hyperkalemia that manifests with electrocardiographic A 27-year-old Caucasian male with a past medical his- findings of an ST segment elevation myocardial infarc- tory of hypertension presented to the emergency room tion (STEMI) is very rare.
    [Show full text]
  • Electrolyte Disorders and Arrhythmogenesis
    Cardiology Journal 2011, Vol. 18, No. 3, pp. 233–245 Copyright © 2011 Via Medica REVIEW ARTICLE ISSN 1897–5593 Electrolyte disorders and arrhythmogenesis Nabil El-Sherif1, Gioia Turitto2 1State University of NY, Downstate Medical Center and NY Harbor VA Healthcare System, Brooklyn, NY, USA 2Methodist University Hospital, Brooklyn, NY, USA Abstract Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mecha- nisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of elec- trolyte disorders. Potassium (K+) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most signifcant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and + non cardiac drugs are known to suppress the HERG K channel and hence the IK, and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricu- lar tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia de- pends on serum K+ level. At 5.5–7.0 mmol/L K+, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K+, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca++) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathy- roidism, results in shortening of both intervals.
    [Show full text]
  • Medical Term Lay Term(S)
    MEDICAL TERM LAY TERM(S) ABDOMINAL Pertaining to body cavity below diaphragm which contains stomach, intestines, liver, and other organs ABSORB Take up fluids, take in ACIDOSIS Condition when blood contains more acid than normal ACUITY Clearness, keenness, esp. of vision - airways ACUTE New, recent, sudden ADENOPATHY Swollen lymph nodes (glands) ADJUVANT Helpful, assisting, aiding ADJUVANT Added treatment TREATMENT ANTIBIOTIC Drug that kills bacteria and other germs ANTIMICROBIAL Drug that kills bacteria and other germs ANTIRETROVIRAL Drug that inhibits certain viruses ADVERSE EFFECT Negative side effect ALLERGIC REACTION Rash, trouble breathing AMBULATE Walk, able to walk -ATION -ORY ANAPHYLAXIS Serious, potentially life threatening allergic reaction ANEMIA Decreased red blood cells; low red blood cell count ANESTHETIC A drug or agent used to decrease the feeling of pain or eliminate the feeling of pain by general putting you to sleep ANESTHETIC A drug or agent used to decrease the feeling of pain or by numbing an area of your body, local without putting you to sleep ANGINA Pain resulting from insufficient blood to the heart (ANGINA PECTORIS) ANOREXIA Condition in which person will not eat; lack of appetite ANTECUBITAL Area inside the elbow ANTIBODY Protein made in the body in response to foreign substance; attacks foreign substance and protects against infection ANTICONVULSANT Drug used to prevent seizures ANTILIPIDEMIC A drug that decreases the level of fat(s) in the blood ANTITUSSIVE A drug used to relieve coughing ARRHYTHMIA Any change from the normal heartbeat (abnormal heartbeat) ASPIRATION Fluid entering lungs ASSAY Lab test ASSESS To learn about ASTHMA A lung disease associated with tightening of the air passages ASYMPTOMATIC Without symptoms AXILLA Armpit BENIGN Not malignant, usually without serious consequences, but with some exceptions e.g.
    [Show full text]
  • Cerebral Salt Wasting: Truths, Fallacies, Theories, and Challenges
    Journal Article Page 1 of 10 Use of this content is subject to the Terms and Conditions of the MD Consult web site. Critical Care Medicine Volume 30 • Number 11 • November 2002 Copyright © 2002 Lippincott Williams & Wilkins REVIEW ARTICLE Cerebral salt wasting: Truths, fallacies, theories, and challenges Sheila Singh, MD; Desmond Bohn, MB; Ana P. C. P. Carlotti; Michael Cusimano, MD; James T. Rutka; Mitchell L. Halperin, MD From the Departments of Pediatric Neurosurgery (SS, JTR) and Critical Care Medicine (DB), Hospital for Sick Children, Toronto, Canada; the Department of Anaesthesiology, University of Toronto, Toronto, Canada (DB); the Department of Pediatrics, Universidade de Sao Paulo, Ribeirao Preto, Brazil (APCPC); and the Department of Neurosurgery (MC) and Renal Division (MLH), St. Michael’s Hospital, University of Toronto, Toronto, Canada. Supported, in part, by a grant from Physicians Services Incorporated. Address requests for reprints to: Mitchell L. Halperin, MD, Division of Nephrology, St. Michael’s Hospital, Annex, 38 Shuter Street, Toronto, Ontario M5B 1A6, Canada. E-mail: [email protected] Cerebral salt wasting is a diagnosis of exclusion that requires a natriuresis in a patient with a contracted effective arterial blood volume and the absence of another cause for this excretion of Na+ . Background: The reported prevalence of cerebral salt wasting has increased in the past three decades. A cerebral lesion and a large natriuresis without a known stimulus to excrete so much sodium (Na+ ) constitute its essential two elements. Objectives: To review the topic of cerebral salt wasting. There is a diagnostic problem because it is difficult to confirm that a stimulus for the renal excretion of Na+ is absent.
    [Show full text]
  • Managing Acute & Chronic Hyperkalemia
    MANAGING ACUTE AND CHRONIC HYPERKALEMIA: SOLVING THE PUZZLE Matthew R. Weir, MD Professor and Chief Division of Nephrology University of Maryland School of Medicine Disclosure Slide Scientific Advisor: Janssen, Astra, BI, MSD, Akebia, Relypsa, Boston Scientific, Lexicon, Bayer, Vifor, CareDx Grant Funding: NIDDK: R01DK066013, U01DK116095,and U01DK106102; NHLBI: R01HL127422, R01HL132732 Outline • Recognition: Review prevalence and risk factors for hyperkaleMia • Management: Review current ManageMent strategies • Treatment: • Describe current approaches for the treatment of hyperkalemia both acutely and chronically • Highlight new option to treat hyperkalemia in patients on renoprotective therapies Overview: Epidemiology of Hyperkalemia • Prevalence in hospitalized patients ranges froM 1%-10% depending on the definition of hyperkaleMia1 • Prevalence in patients with CKD ranges froM 5%-50%, increasing as kidney function declines2 • HyperkaleMia is More coMMon in patients with3 • Reduced kidney function • Multiple medications (especially RAAS inhibitors) • Older age • Diabetes mellitus 1. Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Phys. 2006;73(2):283-290. 2. Reardon LC, Macpherson DS. Arch Intern Med. 1998;158(1):26-32. 3. Lazich I, Bakris G., Semin Nephrol 2014; 34:333-339. Hyperkalemia Varies Widely in Studies and Guidelines • The upper liMit of norMal (ULN) for seruM K+ levels varies across guidelines and publications1-6 Hyperkalemia • Serum K+ levels of 5.0, 5.5, or 6.0 mEq/L are 6.0 commonly used cutoffs for ULN 5.5 • Some studies differentiate hyperkalemia by severity1 + 5.0 • Serum K+ levels ≥5.5-<6.0 mEq/L defined as Normal moderate + (mEq/L) Target Range: K =3.5-5.0 + Serum K 4.0 • Serum K levels ≥6.0 mEq/L defined as severe 3.5 3.0 Hypokalemia K+: potassiuM 1.
    [Show full text]
  • Evaluating and Managing Electrolyte Disbalances in the Outpatient Setting Disclosure
    EVALUATING AND MANAGING ELECTROLYTE DISBALANCES IN THE OUTPATIENT SETTING DISCLOSURE There are no conflicts of interest Homeostasis • Potassium • Water Evaluation and Management of Electrolyte TO BE DISCUSSED Disbalances • Hyperkalemia • Hypokalemia • Hypernatremia • Hyponatremia Summary DISORDERS OF POTASSIUM BALANCE: HYPERKALEMIA AND HYPOKALEMIA POTASSIUM HOMEOSTASIS • Aldosterone • High Na+ delivery to distal tubule Increase (diuretics) Renal K+ • High urine flow (osmotic diuresis) Excretion • High serum K+ level • Delivery bicarbonate to distal tubule • Absence, or very low aldosterone • Low Na+ delivery to the distal Decrease tubule Renal K+ • Low urine flow Excretion • Low serum K+ level • Kidney Injury MORTALITY IN DYSKALEMIA Collins et al Am J Nephrol 2017;46:213- 221 HYPERKALEMIA MY PATIENT HAS HYPERKALEMIA, WHAT SHOULD I DO? H&P and Check other medication causes •Changes? Treat review •Send home •Symptoms? Treat •Metabolic acidosis •Obstruction •Hyperosmolarity •K+ increasing meds •CKD Pseudohyperkale EKG and BMP mia CAUSES OF HYPERKALEMIA Increased potassium release from Reduced urinary potassium excretion cells • Pseudohyperkalemia • Acute and chronic kidney disease • Fist clenching • Reduced aldosterone secretion or • Tourniquet use response to aldosterone • Metabolic acidosis • Reduced distal sodium and water • Insulin deficiency, hyperglycemia, delivery and hyperosmolality • Drugs • Increased tissue catabolism • Drugs • Hyperkalemic Periodic Palasysis Biff Palmer A Physiologic-Based Approach to the Evaluation of a Patient
    [Show full text]
  • Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical Practice Guideline
    Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical Practice Guideline Note: Active Table of Contents – Click each header below to jump to the section of interest Table of Contents INTRODUCTION .................................................................................................................................. 6 DEFINITIONS ....................................................................................................................................... 6 RECOMMENDATIONS ........................................................................................................................ 7 1. POTASSIUM (K+) ............................................................................................................................. 7 3- 2. PHOSPHATE (PO4 ) ........................................................................................................................ 9 3. MAGNESIUM (MG2+) ...................................................................................................................... 10 4. CALCIUM (CA2+) ............................................................................................................................ 12 5. SLIDING SCALE ELECTROLYTES ............................................................................................... 14 METHODOLOGY ............................................................................................................................... 15 COLLATERAL TOOLS & RESOURCES ..........................................................................................
    [Show full text]
  • Hyperkalemia and Hypocalcemia - Literature Review Modalidades De Parada Cardíaca Induzida: Hipercalemia E Hipocalcemia - Revisão De Literatura
    Oliveira MAB,SPECIAL et al. - Modes ARTICLE of induced cardiac arrest: hyperkalemia and Rev Bras Cir Cardiovasc 2014;29(3):432-6 hypocalcemia - Literature review Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - Literature review Modalidades de parada cardíaca induzida: hipercalemia e hipocalcemia - revisão de literatura Marcos Aurélio Barboza de Oliveira1, MD, MsC; Antônio Carlos Brandi2, MD; Carlos Alberto dos Santos2, MD; Paulo Henrique Husseini Botelho2, MD; José Luis Lasso Cortez3, MD; Domingo Marcolino Braile4, MsC, PhD DOI: 10.5935/1678-9741.20140074 RBCCV 44205-1572 Abstract Resumo The entry of sodium and calcium play a key effect on myocyte A entrada de sódio e cálcio desempenham efeito chave no miócito subjected to cardiac arrest by hyperkalemia. They cause cell submetido à parada cardíaca por hiperpotassemia. Eles provocam swelling, acidosis, consumption of adenosine triphosphate and edema celular, acidose, consumo de trifosfato de adenosina e desen- trigger programmed cell death. Cardiac arrest caused by hypo- cadeiam processo de morte celular programada. A parada cardíaca calcemia maintains intracellular adenosine triphosphate levels, provocada por hipocalcemia mantém os níveis intracelulares de improves diastolic performance and reduces oxygen consumption, trifosfato de adenosina, melhora o rendimento diastólico e reduz o which can be translated into better protection to myocyte injury consumo de oxigênio, o que pode ser traduzido em melhor proteção induced by cardiac arrest. do miócito às lesões provocadas pela parada cardíaca induzida. Descriptors: Heart Arrest, Induced. Myocardial Ischemia. Descritores: Parada Cardíaca Induzida. Isquemia Miocárdi- Hyperkalemia. Hypocalcemia. ca. Hiperpotassemia. Hipocalcemia. INTRODUCTION to approach intracardiac diseases[3] by using substances that trigger controlled cardiac arrest, commonly known as cardio- The first cardiac surgeries were performed on a beating plegic agents [4].
    [Show full text]
  • Chapter 73 1009
    C h a p t e r 73 Fluid and Electrolyte Issues in Pediatric Critical Illness Robert Lynch, Ellen Glenn Wood, and Tara M. Neumayr intraoperative fluids influence acid-base and electrolyte status, PEARLS particularly of vulnerable patients.4 The choice of Na+ content • Hypotonic maintenance IV fluids are associated with mild to and balancing ions of IVF for postoperative or critical care moderate hyponatremia in postoperative patients. maintenance may be important for some patients thus justify- Anesthesia, stress, and inflammatory mediators probably ing additional expense. Clearly 0.18 and 0.225 mM saline is 5,6 contribute. Electrolyte monitoring in patients at risk is associated with a higher incidence of mild hyponatremia, essential for detection and management of the occasional although controlled trials do not show this effect for 0.46 mM 7,8 patient who develops severe hyponatremia. This critical saline. Severe hyponatremia has been associated with pul- effect of the syndrome of inappropriate antidiuretic hormone monary or CNS illness in pediatrics and is infrequent even may occur even in patients on isotonic IV fluids. within those categories, with the exception of children with • Medical patients with high levels of inflammatory mediators traumatic brain injury (TBI). Among patients with those and appear to be at increased risk of significant hyponatremia. other illnesses, the evolving study of the influence of inflam- Interleukin effects on antidiuretic hormone release may matory mediators directly on the hypothalamus and indirectly contribute. on vasopressin secretion may further clarify which patients are 9,10 • Albumin infusions have been generally safe but may at most risk of clinically significant hyponatremia.
    [Show full text]
  • YOUR KIDNEYS and HIGH POTASSIUM (HYPERKALEMIA) Are You at Risk?
    YOUR KIDNEYS AND HIGH POTASSIUM (HYPERKALEMIA) Are You At Risk? kidney.org 2 NATIONAL KIDNEY FOUNDATION TABLE OF CONTENTS About Hyperkalemia (High Potassium) What is hyperkalemia? . 4 What causes hyperkalemia? . 5 What are the symptoms of hyperkalemia? . 6 How do I know if I have hyperkalemia? . 6 Treatment for Hyperkalemia Can hyperkalemia be treated? . 7 What is a “normal” level of potassium in blood? . 8 If I have hyperkalemia, should I stop taking my medicines? . 8 What kinds of medicines can cause hyperkalemia? . 9 About Your Diet How much potassium is safe for me to eat? . 11 What are some high-potassium foods? . 12 What are some lower-potassium foods? . 13 What else can I do to keep potassium levels from getting too high? . 14 How do I leach vegetables? . 14 Points to remember . 15 Where can I get more information? . 16 WWW.KIDNEY.ORG 3 About Hyperkalemia What is hyperkalemia? High potassium (called “hyperkalemia”) is a medical problem in which you have too much potassium in your blood . Your body needs potassium . It is an important nutrient that is found in many of the foods you eat . Potassium helps your nerves and muscles, including your heart, work the right way . But too much potassium in your blood can be dangerous . It can cause serious heart problems . 4 NATIONAL KIDNEY FOUNDATION What causes hyperkalemia? The most common causes include: • Kidney disease. Hyperkalemia can happen if your kidneys do not work well . It is the job of the kidneys to balance the amount of potassium taken in with the amount lost in urine .
    [Show full text]