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Respiratory Acidosis Potassium

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 >>

Jci -the Effect Of Acute Respiratory Acidosis On The Internal Equilibrium Of Potassium

Jci -the Effect Of Acute Respiratory Acidosis On The Internal Equilibrium Of Potassium

THE EFFECT OF ACUTE RESPIRATORY ACIDOSIS ON THE INTERNAL EQUILIBRIUM OF POTASSIUM Veterans Administration Hospital, Seattle, Wash. Department of Medicine, University of Washington, Seattle, Wash. Supported by grants from Abbott Laboratories, North Chicago, Illinois, Washington State Fund for Biology and Medicine, and Washington State Heart Association. Find articles by Scribner, B. in: JCI | PubMed | Google Scholar Veterans Administration Hospital, Seattle, Wash. Department of Medicine, University of Washington, Seattle, Wash. Supported by grants from Abbott Laboratories, North Chicago, Illinois, Washington State Fund for Biology and Medicine, and Washington State Heart Association. Find articles by Fremont-Smith, K. in: JCI | PubMed | Google Scholar Veterans Administration Hospital, Seattle, Wash. Department of Medicine, University of Washington, Seattle, Wash. Supported by grants from Abbott Laboratories, North Chicago, Illinois, Washington State Fund for Biology and Medicine, and Washington State Heart Association. Find articles by Burnell, J. in: JCI | PubMed | Google Scholar First published August 1, 1955- More info 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 >>

Dynamics Of Serum Potassium Change During Acute Respiratory Alkalosis

Dynamics Of Serum Potassium Change During Acute Respiratory Alkalosis

, Volume 25, Issue6 , pp 495498 | Cite as Dynamics of serum potassium change during acute respiratory alkalosis In summary, one should be aware that hyperventilation and hypokalaemia occur frequently in the operating room under ordinary clinical conditions. An awareness of the rapidity with which these changes occur, and their extent as well as their potential hazards, should cause consideration of more aggressive attempts to maintain normocarbia and to use supplemental potassium during anaesthesia, particularly in patients with cardiac disease. Metabolic AcidosisSerum PotassiumHypokalemiaAcid Base BalanceSerum Potassium Level These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. Ce travail est un rappel de la frquence des situations hyperventilation et hypokalimie dans la pratique anesthsique courante. La ralisation de la rapidit avec laquelle surviennent ces changements, de leur importance et de leurs complications possibles, devrait nous rendre plus attentifs au maintien de la normocarbie et celui de la normokalimie par administration de cet lectrolyte en cours anesthsie. Tout ceci est encore vrai chez le malade cardiaque et hypertendu qui reoivent de la digitale ou des diurtiques. Anderson, H.N. &Savane, H. Pattern of biochemical response to acute changes in PaC02. Ann. Surg.156: 752 (1962). CrossRef Google Scholar Hall, K.D. &Reeser, F.H. Serum potassium levels in hyperventilated dogs. Proc. Soc. Exper. Biol. Med.111: 251 (1962). Google Scholar Flemma, R.J. &Young, W.G. The metabolic effects of mechanical ventilation and respiratory alkalosis in post-operative patients. Surgery56: (1) 36 (1964). PubMed Google Scholar Eichenholz, A. Respiratory alkalosis. Arch. I 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

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 >>

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 >>

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 >>

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 >>

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 >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus 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 >>

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 >>

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 >>

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 >>

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