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Why Does Potassium Increase In Metabolic Acidosis?

Potassium Jeremy E. Kaslow, M.d.

Potassium Jeremy E. Kaslow, M.d.

Potassium is an extremely valuable electrolyte essential to heart and kidney function as well as to the maintenance of blood and urine pH. It is the chief electrolyte in the fluid of cells. In fact, only a small part of the total body potassium is contained in the serum. Serum potassium values range from 3.5 to 5.0 mmol/L while the concentration inside the red blood cell is at least l5 to 20 times this amount. While only a part of the total body potassium is found in the serum, proper serum values are critical to normal physiology, especially adrenal, heart and renal functions. Potassium should always be viewed in relation to the other electrolytes. Adrenal Cortex under function. With hypoadrenia, you may get dizzy when you sit or stand quickly, fatigue (especially feeling tired in the morning), crave salt or salty foods, have a low systolic blood pressure, experience food and/or environmental sensitivities, feel weak or tired after colds, stress or exercise, sweat easily with exertion, get shortness of breath after very minimal exertion even though you are in shape, get colds and upper respiratory tract infections easily, etc. Aldosterone is produced by the adrenal cortex, with insufficient production, the body loses sodium in the urine in exchange for potassium. This is why you may see a relatively low sodium with a relative elevated serum potassium with adrenal cortex underactivity. The adrenal corticosteroids also favor the anabolic over catabolic balance. With less effect, there is less potassium in the cell and more in the serum. Catabolic/Dysaerobic State. See aerobic metabolism webpage for more about this. Metabolic Acidosis. The level in the serum goes up while the level inside the cell goes down as the potassium is pumped out of the cell in exchange for the e Continue reading >>

Metabolic Acidosis - An Overview | Sciencedirect Topics

Metabolic Acidosis - An Overview | Sciencedirect Topics

Metabolic acidosis is a process that leads to the accumulation of H+ ions and the decrease in the content of HCO3 ions in the body. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Metabolic acidosis is the most common acid-base disorder recognized in domestic animals. Like in respiratory alkalosis (see Chapter 91), the bicarbonate buffer equation is shifted to the left in metabolic acidosis (Fig. 87-1). Also, with an excess acid load or decreased urinary acid excretion, either an increased or normal plasma AG can be seen (see Table 86-1). What determines whether the AG will increase in metabolic acidosis? Whenever H+ is added to the system, HCO3 is consumed. The hydrogen cation cannot be added without an anion. Therefore, for each HCO3 consumed, a negative charge of some other type (which accompanied the H+) is added to body fluids. If the anion happens to be Cl, no change in the AG will develop. However, if it is any other anion, the AG will be increased. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 What is the cause of the metabolic acidosis in this patient? Metabolic acidosis in this patient was not simply the result of loss of NaHCO3 in diarrheal fluid because the PAnion gap was 26 mEq/L. L-Lactic acidosis is unlikely because there was no hemodynamic problem, liver function tests were normal, and the time period was too short for a nutritional deficiency (e.g., thiamin and/or riboflavin deficiency) that may have caused L-lactic acidosis. Moreover, he did not ingest drugs that may be associated with L-lactic acidosis. There was no history of diabetes mellitus or the intake of ethanol, and his blood sugar was normal. Later, L-lactic acidosis Continue reading >>

Fluids And Electrolyte Management, Part 2

Fluids And Electrolyte Management, Part 2

Etiology. Gastroenteritis is the most common cause of pediatric hypokalemia.1 Pathophysiology. Potassium is an intracellular ion whose concentration is regulated by multiple mechanisms: Alkalosis shifts potassium into cells and acidosis shifts it out. For every increase in pH by 0.1 unit, serum potassium drops by 1 mEq/L. Insulin shifts potassium into cells via a sodium-potassium ATPase pump. Potassium excretion from the kidneys is regulated by aldosterone, mineralocorticoids, antidiuretic hormone, urinary flow rate, metabolic alkalosis, and sodium delivery to the distal tubules. Specific illnesses will lower the serum potassium in different ways. Diarrhea results in the loss of potassium through the gastrointestinal tract. However, vomiting does not directly cause hypokalemia through gastrointestinal losses, but results in alkalosis secondary to the loss of gastric fluids and volume loss, and the alkalosis increases potassium excretion from the kidneys. Hypovolemia (releasing aldosterone), diuretics, genetic renal tubular disorders, and osmotic diuresis (e.g., glucosuria) all increase the secretion of potassium via the renal tubules. (See Table 2.)1,2,3 TABLE 2. ETIOLOGY OF PEDIATRIC HYPOKALEMIA2,3 Hypokalemia affects many organs since it causes cellular dysfunction. The main organs affected are the muscles (rhabdomyolysis), heart, nervous system, and kidneys. Clinical Features. History. Once hypokalemia is established, a detailed history to identify the potential cause is important. A history of diarrhea or vomiting can easily establish the cause without having to do an extensive workup. Ask about medication use and changes in enteral or parenteral formulation, such as total parenteral nutrition (TPN). Symptoms of hypokalemia typically are not seen at a serum level o Continue reading >>

Metabolic Acidosis: Practice Essentials, Background, Etiology

Metabolic Acidosis: Practice Essentials, Background, Etiology

Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. An acid is a substance that can donate hydrogen ions (H+). A base is a substance that can accept H+ ions. The ion exchange occurs regardless of the substance's charge. Strong acids are those that are completely ionized in body fluids, and weak acids are those that are incompletely ionized in body fluids. Hydrochloric acid (HCl) is considered a strong acid because it is present only in a completely ionized form in the body, whereas carbonic acid (H2 CO3) is a weak acid because it is ionized incompletely, and, at equilibrium, all three reactants are present in body fluids. See the reactions below. The law of mass action states that the velocity of a reaction is proportional to the product of the reactant concentrations. On the basis of this law, the addition of H+ or bicarbonate (HCO3-) drives the reaction shown below to the left. In body fluids, the concentration of hydrogen ions ([H+]) is maintained within very narrow limits, with the normal physiologic concentration being 40 nEq/L. The concentration of HCO3- (24 mEq/L) is 600,000 times that of [H+]. The tight regulation of [H+] at this low concentration is crucial for normal cellular activities because H+ at higher concentrations can b Continue reading >>

On The Relationship Between Potassium And Acid-base Balance

On The Relationship Between Potassium And Acid-base Balance

The notion that acid-base and potassium homeostasis are linked is well known. Students of laboratory medicine will learn that in general acidemia (reduced blood pH) is associated with increased plasma potassium concentration (hyperkalemia), whilst alkalemia (increased blood pH) is associated with reduced plasma potassium concentration (hypokalemia). A frequently cited mechanism for these findings is that acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. As a recently published review makes clear, all the above may well be true, but it represents a gross oversimplification of the complex ways in which disorders of acid-base affect potassium metabolism and disorders of potassium affect acid-base balance. The review begins with an account of potassium homeostasis with particular detailed attention to the renal handling of potassium and regulation of potassium excretion in urine. This discussion includes detail of the many cellular mechanisms of potassium reabsorption and secretion throughout the renal tubule and collecting duct that ensure, despite significant variation in dietary intake, that plasma potassium remains within narrow, normal limits. There follows discussion of the ways in which acid-base disturbances affect these renal cellular mechanisms of potassium handling. For example, it is revealed that acidosis decreases potassium secretion in the distal renal tubule directly by effect on potassium secretory channels and indirectly by increasing ammonia production. The clinical consequences of the physiological relation between acid-base and potassium homeostasis are addressed under three headings: Hyperkalemia in Acidosis; Hypokalemia w Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Payperview: Serum Potassium Concentration In Acidemic States - Karger Publishers

Payperview: Serum Potassium Concentration In Acidemic States - Karger Publishers

Serum Potassium Concentration in Acidemic States I have read the Karger Terms and Conditions and agree. It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4CI- or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undert Continue reading >>

Potassium Increase Or Decrease With Metabolic Acidosis, Confused?

Potassium Increase Or Decrease With Metabolic Acidosis, Confused?

Potassium increase or decrease with metabolic acidosis, confused? Ok in metabolic acidosis, renal compensation is increase in aldosertone, which cause hydrogen and potassium excretion leading to hypokalemia. But in metabolic acidosis transcellular movement occurs and there is hyperkalemia. What is the final result for potassium level. Hyper or hypo? Ok in metabolic acidosis, renal compensation is increase in aldosertone, which cause hydrogen and potassium excretion leading to hypokalemia. But in metabolic acidosis transcellular movement occurs and there is hyperkalemia. What is the final result for potassium level. Hyper or hypo? Which one do you think? You just said "renal compensation" which is relatively slow. The final result, or at least the desired result, is physiologic acid-base neutrality (pH 7.35-7.45) and normal serum potassium levels. Since you haven't responded, I can only assume you've posted a question, but are not interested in entering into a discussion of the issues involved in arriving at an answer. Others might be interested so I'll elaborate. In primary metabolic acidosis, the initial response is the movement of H+ ions into cells in exchange for K+ ions, as you said. This can lead to hyperkalemia but it does not affect total body potassium. The main compensatory response for metabolic acidosis is usually respiratory; accomplished by a degree of hyperventilation to expel CO2. This shifts the reaction:CO2+H2O <-> H2CO3 to the left thus decreasing carbonic acid levels and producing a secondary respiratory alkalosis. This will usually compensate for the primary acidosis up to about pH 7.2. As the pH normalizes, K+ returns to the cells in exchange for H+ (actually hydronium ions). The kidneys accomplish the final adjustment of pH, but would not be expe Continue reading >>

The Plasma Potassium Concentration In Metabolic Acidosis: A Re-evaluation

The Plasma Potassium Concentration In Metabolic Acidosis: A Re-evaluation

Volume 11, Issue 3 , March 1988, Pages 220-224 The Plasma Potassium Concentration in Metabolic Acidosis: A Re-evaluation Get rights and content The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCl infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone). Continue reading >>

The Plasma Potassium Concentration In Metabolic Acidosis: A Re-evaluation

The Plasma Potassium Concentration In Metabolic Acidosis: A Re-evaluation

Volume 11, Issue 3 , March 1988, Pages 220-224 The Plasma Potassium Concentration in Metabolic Acidosis: A Re-evaluation Get rights and content The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCl infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone). Continue reading >>

Effect Of Metabolic Acidosis On Renal Tubular Sodium Handling In Rats As Determined By Lithium Clearance

Effect Of Metabolic Acidosis On Renal Tubular Sodium Handling In Rats As Determined By Lithium Clearance

PrintversionISSN 0100-879XOn-lineversionISSN 1414-431X Braz J Med Biol Resvol. 31n. 10Ribeiro PretoOct.1998 Braz J Med Biol Res, October 1998, Volume 31(10) 1269-1273 (Short Communication) Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance L.F. Menegon1, J.F. Figueiredo2 and J.A.R. Gontijo1 1Disciplina de Medicina Interna, Laboratrio de Balano Hidro-Salino, and 2Disciplina de Nefrologia, Laboratrio de Conservao de rgos, Ncleo de Medicina e Cirurgia Experimental, Departamento de Clinica Mdica, Faculdade de Cincias Mdicas, Universidade Estadual de Campinas, Campinas, SP, Brasil Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in male Wistar-Hannover rats (200-250 g). Chronic acidosis (pH 7.16 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 36.4%), accompanied by an increase in fractional proximal (113.3 3.6%) and post-proximal (179.7 20.2%) Na+ and urinary K+ (163.4 5.6%) excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. A lower final body weight was observed in the acidotic (232 4.6 g) and pair-fed (225 3.6 g) rats compared to the controls (258 3.7 g). In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 0.05 g) compared to the other experimental groups (control, 1.46 0.05 g; pair-fed, 1.4 0.05 g). We suggest that altered renal Na+ and K+ handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transp Continue reading >>

Effects Of Ph On Potassium: New Explanations For Old Observations

Effects Of Ph On Potassium: New Explanations For Old Observations

Go to: Abstract Maintenance of extracellular K+ concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle. Potassium homeostasis during intermittent ingestion of K+ involves rapid redistribution of K+ into the intracellular space to minimize increases in extracellular K+ concentration, and ultimate elimination of the K+ load by renal excretion. Recent years have seen great progress in identifying the transporters and channels involved in renal and extrarenal K+ homeostasis. Here we apply these advances in molecular physiology to understand how acid-base disturbances affect serum potassium. The effects of acid-base balance on serum potassium are well known.1 Maintenance of extracellular K+ concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle.2 However, maintenance of normal extracellular K+ (3.5 to 5 mEq/L) is under two potential threats. First, as illustrated in Figure 1, because some 98% of the total body content of K+ resides within cells, predominantly skeletal muscle, small acute shifts of intracellular K+ into or out of the extracellular space can cause severe, even lethal, derangements of extracellular K+ concentration. As described in Figure 1, many factors in addition to acid-base perturbations modulate internal K+ distribution including insulin, catecholamines, and hypertonicity.3,4 Rapid redistribution of K+ into the intracellular space is essential for minimizing increases in extracellular K+ concentration during acute K+ loads. Second, as also illustrated in Figure 1, in steady state the typical daily K+ ingestion of about 70 mEq/d would be sufficient to cause large changes in extracellular K+ were it not for Continue reading >>

Hypokalaemia And Metabolic Acidosis

Hypokalaemia And Metabolic Acidosis

Home | Education | Hypokalaemia and Metabolic Acidosis 35 year old Aboriginal female presents with a 2/52 Hx of weakness, thirst and nausea. Presents to ED unable to lift her hands. Admitted 3/12 ago with something similar but doesnt know what it was and her medical notes are not immediately available. No other past medical history of note. Examination reveals a quiet, dehydrated lady with generalised non-lateralising weakness in all 4 limbs. Bedside venous blood gas results included: Sinus rhythm with sinus arrhythmia at a rate of 72 bpm. U waves noted most prominently in leads V1-V3 Sinus arrhythmia [sinus rhythm with slight variation (>0.16 seconds) in the sinus cycles] Normal anion gap metabolic acidosis. The 2 most common causes in ED Other causes are many and varied. There are several mnemonics out there the most recent edition of Rosen suggests: F-USED CARS Basically (and rather obviously), a metabolic acidosis is caused by either excess acid or a loss of alkali. Excess acid may be produced by the body itself or may be exogenous. Calculating the anion gap is used in the context of having made a diagnosis of a metabolic acidosis to help determine possible causes. Its an artificial but pragmatic concept based on the fact that with normal physiology there will be more unmeasured anions (predominantly Albumin, Phosphate and Sulphate) than cations on routine blood testing. Most people dont use potassium in the equation resulting in a normal range of 8-12. (12-16 if potassium included), although in this case it wouldnt have made much difference! A wide anion gap in the setting of a metabolic acidosis (or High Anion Gap Metabolic Acidosis [HAGMA]) suggests there is excess unmeasured anion / acid. Keeping it simple, there are only 4 causes: Essentially a state of excess Continue reading >>

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems. Hyperventilation ( Kussmaul respirations ) - this is the compensatory response Shift of oxyhaemoglobin dissociation curve (ODC) to the right Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold) Resistance to the effects of catecholamines Increased bone resorption (chronic acidosis only) Shift of K+ out of cells causing hyperkalaemia 5.4.2 Some Effects have Opposing Actions. The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates. The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually rises during acidosis. The shift of the oxygen dissociation curve to the right due to the acidosis occurs rapidly. After 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Acidosis is commonly said to cause hyperkalaemia by a shift of potassium out of cells. The effect on potassium levels is extremely variable and indirect effects due to the type of acidosis present are much more important. For example hyperkalaemia is due to renal failure in uraemic acidosis rather than the acidosis. Significant potassium loss du Continue reading >>

Metabolic Acidosis And Alkalosis

Metabolic Acidosis And Alkalosis

Page Index Metabolic Acidosis. Metabolic Alkalosis Emergency Therapy Treating Metabolic Acidosis Calculating the Dose Use Half the Calculated Dose Reasons to Limit the Bicarbonate Dose: Injected into Plasma Volume Fizzes with Acid Causes Respiratory Acidosis Raises Intracellular PCO2 Subsequent Residual Changes Metabolic Acidosis. The following is a brief summary. For additional information visit: E-Medicine (Christie Thomas) or Wikepedia Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap: Metabolic Acidosis with a Normal Anion Gap: Longstanding diarrhea (bicarbonate loss) Uretero-sigmoidostomy Pancreatic fistula Renal Tubular Acidosis Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants Renal failure Metabolic Acidosis with an Elevated Anion Gap: lactic acidosis ketoacidosis chronic renal failure (accumulation of sulfates, phosphates, uric acid) intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin. rhabdomyolysis For further details visit: E-Medicine (Christie Thomas). Treating Severe Metabolic Acidosis. The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required: Metabolic Alkalosis Etiology: Primary Metabolic alkalosis may occur from various causes including: Loss of acid via the urine, stools, or vomiting Transfer of Continue reading >>

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