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How Does Respiratory Acidosis Cause Hyperkalemia

Serum Potassium Concentration In Acidemic States.

Serum Potassium Concentration In Acidemic States.

Serum potassium concentration in acidemic states. It has been generally accepted that acidosis results in hyperkalemia because ofshifts of potassium from the intracellular to the extracellular compartment.There is ample clinical and experimental evidence, however, to support theconclusion that uncomplicated organic acidemias do not produce hyperkalemia. Inacidosis associated with mineral acids (respiratory acidosis, end-stage uremicacidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results inpredictable increases in serum potassium concentration. In acidosis associatedwith nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary tomethylmalonic and isovaleric acids, and ethylene glycol, paraldehyde andsalicylate intoxications), serum potassium concentration usually remains withinthe normal range in uncomplicated cases. A number of factors, however, may beresponsible for hyperkalemia in some of these patients other than the acidemiaper se. These include dehydration and renal hypoperfusion, preexisting renaldisease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status ofpotassium balance, and therapy. The mechanism(s) of this differing effect ofmineral and organic acidemias on transmembrane movement of potassium remainsundefined. The prevalent hypothesis, however, favors the free penetrance of theorganic anion into cells without creating a gradient for the hydrogen ions and,thus, obviating the efflux of intracellular potassium. The importance of thepresence of hyperkalemia in clinical states of organic acidemias is obvious. Asearch for the complicating factors reviewed above should be undertaken sinceorganic acidemias per se, should not be expected to be accompanie Continue reading >>

Hypokalemia And Respiratory Acidosis

Hypokalemia And Respiratory Acidosis

Hello. I just wanted to get your inputs on this scenario: Hyperkalemia is frequently associated with acidosis as potassium moves out of the cell to compensate for hydrogen moving into the cell. How, then, would you explain the patients hypokalemia occurring along with respiratory acidosis? (Hint: The patient is concurrently receiving Potassium Chloride 40 mEq/L in IV fluid. Actually, if hydrogen is moving into the cells that would make it alkalosis because hydrogen would be leaving the blood. The pH of blood depends on two things: the amount of hydrogen ions and the amount of bicarbonate (HCO3). Most of the time you can determine the type of acid-base imbalance by the substance that is most outside its normal limits. Usually metabolic is associated with bicarb whereas respiratory is tied to hydrogen. That being said, I'm not sure how you might be having HYPOkalemia when you're having a potassium drip. You might need to share a little more info about the patient/problem before getting a good answer. I'm not sure I helped any with that answer... can't. respiratory acidosis is always due to an inadequate exhalation of c02. this causes the co2 levels in the blood to elevate (normal arterial co2 is 35-45 mmhg) and carbonic acid levels in the blood to increase. as well, the person often hypoventilates which results in low o2 levels. this patient's respiratory acidosis does not explain their hypokalemia. the only way respiratory acidosis and hypokalemia could be related is if the patient had some medical condition in addition to the respiratory acidosis that had hypokalemia as one of its features or complications. so, some other pathophysiology is going on. 40 meq of kcl is commonly added to a liter of iv fluids and is done for potassium replacement purposes. 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 >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [ 1 ] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis , Metabolic Acidosis , and Pediatric Metabolic Acidosis .) Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following: Central nervous system disease or drug-induced r Continue reading >>

Renal Compensation

Renal Compensation

Chronic Carbon Dioxide Retainer Renal compensation of respiratory acidosis is by increased urinary excretion of hydrogen ions and resorption of HCO3−. This relatively slow process occurs over several days. Slowly, pH reaches low normal values, but HCO3− levels and BE are increased. This is the situation of the patient with chronic respiratory failure. Pulmonary patients usually have chronic obstructive pulmonary disease or restrictive pulmonary disease, or they are morbidly obese. Increased Co2 stores are the rule, and the normal respiratory drive to Paco2 is obtunded. This group of patients is sensitive to O2 supplementation because respiratory drive is predominantly determined by hypoxemia. Patients with a Pao2 in the mid-50s and a Paco2 at the same level usually receive home O2 treatment, initially at night to reduce pulmonary hypertension and to relieve dyspnea. When the chronic Co2 retainer develops an acute respiratory problem and pH levels fall to less than 7.20, noninvasive ventilatory assistance is usually indicated. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, a Continue reading >>

Hypercapnia, Hyperkalemia, Respiratory Acidosis: Causes & Diagnoses | Symptoma.com

Hypercapnia, Hyperkalemia, Respiratory Acidosis: Causes & Diagnoses | Symptoma.com

[] regional hyperinflation oxygenation target: SpO2 90%, PaO2 60mmHg carbon dioxide target: ARDSnet aimed for a normal CO2 - but lung is exposed to repeated tidal stretch, ideally hypercapnia [lifeinthefastlane.com] Respiratory alkalosis may be present early in the course of the disease; hypercarbia and respiratory acidosis develop as the disease progresses. [amfs.com] With this type of ventilation, higher levels of CO 2 can be tolerated ( permissive hypercapnia ). [amboss.com] [] tested, but it also generated high inspiratory pressures, between 25 and 30cm H 2 O, despite the selection of a minimal tidal volume (5ml/kg) and the use of permissive hypercapnia [bmcpediatr.biomedcentral.com] Disruption of the subunit of the epithelial Na channel in mice: hyperkalemia and neonatal death associated with a pseudohypoaldosteronism phenotype . [nature.com] Prolonged or difficult parturition can cause acidosis in the foal which can also lead to respiratory distress. [vetstream.com] The ECG manifestations of hyperkalemia begin with peaked T waves. [foamcast.org] acidosis from hypoxia and metabolic acidosis secondary to lactic acid generation from poor tissue perfusion, impaired hepatic metabolism, and reduced acid excretion. 3, 10 [nursingcenter.com] Contraindications to resuscitation include: - Avalanche burial 35 minutes with airway packed with snow and initial rhythm of asystole -Asphyxiation - Hyperkalemia ( 12 mmol [ems1.com] Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure, and a propensity toward arrhythmias . [4] [5] Hypercapnia may increase pulmonary [en.wikipedia.org] In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia . [en.wikipedia.org] Aci Continue reading >>

Potassium And Acidosis

Potassium And Acidosis

Balance among electrically charged atoms and molecules is essential to maintaining chemical equilibrium in your body. Potassium is the most abundant, positively charged atom inside your cells. Because acids and potassium both have a positive electrical charge in your body, their concentrations are interdependent. Medical conditions that cause an overabundance of acids in your blood, known as acidosis, may affect your blood potassium level, and vice versa. Video of the Day Metabolic acidosis is an abnormally low blood pH caused by overproduction of acids or failure of your kidneys to rid the body of acids normally. With metabolic acidosis, your blood has an abnormally high level of positively charged hydrogen atoms, or hydrogen ions. To reduce the acidity of your blood, hydrogen ions move from your circulation into your cells in exchange for potassium. The exchange of hydrogen for potassium ions helps relieve the severity of acidosis but may cause an abnormally high level of blood potassium, or hyperkalemia. Drs. Kimberley Evans and Arthur Greenberg reported in a September 2005 article published in the "Journal of Intensive Care Medicine" that there is a 0.3 to 1.3 mmol/L increase in blood potassium for every 0.1 decrease in pH with metabolic acidosis. Metabolic Acidosis Recovery Correction of the underlying medical problem responsible for metabolic acidosis typically leads to normalization of your blood pH. Although blood potassium is typically elevated with metabolic acidosis, a substantial amount of your total body potassium stores can be lost through the kidneys, causing a total body deficit. As your blood pH returns to normal, potassium moves from your bloodstream back into your cells. If your total body potassium stores have been depleted, your blood concentration Continue reading >>

Effects Of Ph On Potassium: New Explanations For Old Observations

Effects Of Ph On Potassium: New Explanations For Old Observations

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 continuous renal K+ excretion, because K+ loss from the gastrointestinal tract is quite modest under normal conditions. Thus, plasma K+ is at the mercy of the interplay between internal K+ distribution and external K+ balance mediated by renal K+ excretion. Recent years have seen remarkable advances in identifying the transport processes involved in renal and extrarenal K+ balance and their regulation. Here we apply these advances in molecular physiology to understand the basis for longstanding observations of the effects of acid-base disturbances on serum potassium. We do not address the large spectrum of clinical syndromes that mutually affect K+ and acid-base 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 >>

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 >>

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 >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

Acidosis - An Overview | Sciencedirect Topics

Acidosis - An Overview | Sciencedirect Topics

Acidosis is an important prognostic factor in survival from respiratory failure during COPD exacerbation, and thus early correction of acidosis is an essential goal of therapy. Katherine Ahn Jin, in Comprehensive Pediatric Hospital Medicine , 2007 Acidosis is defined as an abnormal clinical process that causes a net gain in hydrogen ions (H+) in the extracellular fluid. Metabolic acidosis occurs when there is an accumulation of H+ or a loss of bicarbonate ions (HCO3) and is reflected by a decrease in plasma HCO3 (<22 mEq/L). Respiratory acidosis occurs when there is an accumulation of carbon dioxide (CO2) and is reflected by an increase in the arterial partial pressure of carbon dioxide (Pco2 >40 mm Hg). Clinically, acid-base scenarios can involve a primary acidosis or alkalosis with or without compensation, or a mixed acid-base disorder. The pH reflects the net effect of these processes (Fig. 27-1). The term acidemia is defined as an abnormal decrease in blood pH (<7.37). Sharma S. Prabhakar M.D., M.B.A., F.A.C.P., F.A.S.N., in Medical Secrets (Fifth Edition) , 2012 What is the conceptual difference between an AG and a non-AG metabolic acidosis? An AG acidosis is caused by the addition of a nonvolatile acid to the ECF. Examples include diabetic ketoacidosis, lactic acidosis, and uremic acidosis. A non-AG acidosis commonly (but not exclusively) represents a loss of . Examples include lower GI losses from diarrhea and urinary losses due to renal tubular acidosis (RTA). Therefore, when approaching a patient with an AG acidosis, one should look for the source and identity of the acid gained. By contrast, when evaluating a patient with a non-AG acidosis, one should begin by looking for the source of the Mario G. Bianchetti, Alberto Bettinelli, in Comprehensive Pediatric Ne Continue reading >>

Potassium Balance In Acid-base Disorders

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>

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