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Fractional Excretion of Bicarbonate

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101. Toxicity, Barbiturate (Treatment)

to be renally excreted. Urinary alkalinization is not recommended for short-acting barbiturates. Enhancement of urinary elimination may be accomplished with an initial sodium bicarbonate bolus of 1 mEq/kg followed by a constant infusion. This infusion may be made by adding 100-150 mEq of sodium bicarbonate to 850 mL of D5 and titrating to maintain a urine pH of greater than 7.5 with an arterial pH of less than 7.50. The goal should be a urine output of 150-250 mL/h. Risks include hypokalemia, fluid overload (...) it was administered at 30 minutes, 60 minutes, and 120 minutes, respectively, current guidelines in overdose management question its benefit. There is no evidence that the administration of activated charcoal improves clinical outcome. Indeed, its use has decreased to less than 5% of all reported ingestions in recent years. [ ] A single dose of activated charcoal may be given within an hour of overdose if the clinician estimates that a clinically significant fraction of the ingested substance remains in the GI

2014 eMedicine.com

102. Respiratory Acidosis (Overview)

elevates plasma bicarbonate values, but only slightly (approximately 1 mEq/L for each 10-mm Hg increase in PaCO 2 ). The second step is renal compensation that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased, and bicarbonate reabsorption is increased. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: Acute respiratory acidosis – Bicarbonate increases by 1 mEq/L for each 10-mm Hg rise in PaCO 2 (...) hypoventilation leads to an increased PaCO 2 (ie, hypercapnia). The increase in PaCO 2 , in turn, decreases the bicarbonate (HCO 3 – )/PaCO 2 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

2014 eMedicine.com

103. Respiratory Alkalosis (Overview)

quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide. [ ] The carbon dioxide combines with water to form carbonic acid. The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. Significant alterations in ventilation can affect the elimination of carbon dioxide and lead to a respiratory acid-base disorder. PaCO 2 is normally maintained in the range (...) 03, 2018 Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP Share Email Print Feedback Close Sections Sections Respiratory Alkalosis Overview Background Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO 2 ). In turn, the decrease in PaCO 2 increases the ratio of bicarbonate concentration to PaCO 2 and, thereby, increases the pH

2014 eMedicine.com

104. Syndrome of Inappropriate Secretion of Antidiuretic Hormone (Overview)

, the nonphysiological secretion of AVP results in enhanced water reabsorption, leading to dilutional hyponatremia. While a large fraction of this water is intracellular, the extracellular fraction causes volume expansion. Volume receptors are activated and natriuretic peptides are secreted, which causes natriuresis and some degree of accompanying potassium excretion (kaliuresis). Eventually, a steady state is reached and the amount of Na + excreted in the urine matches Na intake. Ingestion of water is an essential (...) of the antidiuretic hormone arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion. [ ] The key to understanding the pathophysiology, signs, symptoms, and treatment of SIADH is the awareness that the results from an excess of water rather than a deficiency of sodium. Signs and symptoms Depending on the magnitude and rate of development, hyponatremia may or may not cause symptoms. The history should take into account the following considerations: In general

2014 eMedicine.com

105. Metabolic Acidosis (Overview)

. Comparison of Types 1, 2, and 4 RTA Characteristics Proximal (Type 2) Distal (Type 1) Type 4 Primary defect Proximal HCO 3 - reabsorption Diminished distal H+ secretion Diminished ammoniagenesis Urine pH < 5.5 when serum HCO 3 - is low >5.5 < 5.5 Serum HCO 3 - >15 mEq/L Can be < 10 mEq/L >15 mEq/L Fractional excretion of HCO 3 - (FEHCO 3 ) >15-20% during HCO 3 - load < 5% (can be as high as 10% in children) < 5% Serum K + Normal or mild decrease Mild-to-severe decrease* High Associated features Fanconi (...) concentrations. On the basis of this law, the addition of H + or bicarbonate (HCO 3 - ) drives the reaction shown below to the left. H 2 CO 3 (acid)↔H + + HCO 3 - (base) 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 HCO 3 - (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

2014 eMedicine.com

106. Hyperkalemia (Overview)

(eg, increased intake or inhibited excretion) In patients with severe hyperkalemia, treatment is as follows: IV calcium to ameliorate cardiac toxicity, if present Identify and remove sources of potassium intake IV glucose and insulin infusion to enhance potassium uptake by cells Correct severe metabolic acidosis with sodium bicarbonate Consider beta-adrenergic agonist therapy (eg, nebulized albuterol, 10 mg, administered by a respiratory therapist); preferred over alkali therapy in patients (...) delivery to the distal tubule (eg, diuretics) High urine flow (eg, osmotic diuresis) High serum potassium level Delivery of negatively charged ions to the distal tubule (eg, bicarbonate) Renal potassium excretion is decreased by the following: Absence, or very low levels, of aldosterone WNK1 and WNK4 mutations Low sodium delivery to the distal tubule Low urine flow Low serum potassium level Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high

2014 eMedicine.com

107. Hyperchloremic Acidosis (Overview)

, urinary loss of glucose, amino acids, phosphate, uric acid, and other organic anions, such as citrate, can also occur (Fanconi syndrome). A distinctive feature of type II pRTA is that it is nonprogressing, and when the serum bicarbonate is reduced to approximately 15 mEq/L, a new transport maximum for bicarbonate is established and the proximal tubule is able to reabsorb all of the filtered bicarbonate. A fractional excretion of bicarbonate (FE[HCO 3 - ]) greater than 15% when the plasma bicarbonate (...) is normal after bicarbonate loading is diagnostic of pRTA. In contrast, the fractional excretion of bicarbonate in low and normal bicarbonate levels is always less than 5% in distal RTA (dRTA). Another feature of pRTA is that the urine pH can be lowered to less than 5.5 with acid loading. The pathogenic mechanisms responsible for the tubular defect in persons with pRTA are not completely understood. Defective pump secretion or function, namely aberrations in the function of the proton pump ([H

2014 eMedicine.com

108. Hypocitraturia (Overview)

filtration rate (GFR) decreases, there is a stepwise decrease in the amount of citrate that is filtered; however, in the early stages of CKD, the increased fractional excretion of citrate prevents an abrupt decline in urinary citrate, such that overt hypocitraturia is not usually observed until advanced stages of CKD. [ ] Primary Hyperaldosteronism In this disease entity, both hypercalciuria and hypocitraturia occur via Na-dependent volume expansion and chronic hypokalemia. [ ] Previous Next: US (...) . Urol Res . 2006 Aug. 34(4):231-8. . Kessler T, Hesse A. Cross-over study of the influence of bicarbonate-rich mineral water on urinary composition in comparison with sodium potassium citrate in healthy male subjects. Br J Nutr . 2000 Dec. 84(6):865-71. . Pinheiro VB, Baxmann AC, Tiselius HG, Heilberg IP. The effect of sodium bicarbonate upon urinary citrate excretion in calcium stone formers. Urology . 2013 Jul. 82(1):33-7. . Seltzer MA, Low RK, McDonald M. Dietary manipulation with lemonade

2014 eMedicine.com

109. Hypocalcemia (Overview)

: Pathophysiology Ionized calcium is the necessary plasma fraction for normal physiologic processes. In the neuromuscular system, ionized calcium facilitates nerve conduction, muscle contraction, and muscle relaxation. Calcium is necessary for bone mineralization and is an important cofactor for hormonal secretion in endocrine organs. At the cellular level, calcium is an important regulator of ion transport and membrane integrity. Calcium turnover is estimated to be 10-20 mEq/day. Approximately 500 mg (...) of calcium is removed from the bones daily and replaced by an equal amount. Normally, the amount of calcium absorbed by the intestines is matched by urinary calcium excretion. Despite these enormous fluxes of calcium, the levels of ionized calcium remain stable because of the rigid control maintained by parathyroid hormone (PTH), vitamin D, and calcitonin through complex feedback loops. These compounds act primarily at bone, renal, and GI sites. Calcium levels are also affected by magnesium

2014 eMedicine.com

110. Milk-Alkali Syndrome (Overview)

and bicarbonate, for treatment of peptic ulcer disease. (See Pathophysiology, Etiology, Prognosis, Presentation, and Workup.) [ ] With the development of nonabsorbable alkali and histamine-2 blockers for treatment of peptic ulcer disease, milk-alkali syndrome became a rare cause of hypercalcemia; however, with the increased use and promotion of calcium carbonate for dyspepsia and for calcium supplementation, a resurgence of milk-alkali syndrome has occurred. (See Etiology and Epidemiology.) A few authors (...) . Adaptation of intestinal calcium absorption to oral intake may play a role and help to explain individual variability in the development of milk-alkali syndrome. Some persons maintain a high fractional absorption of calcium even with a high intake, while other persons decrease fractional absorption with a high intake. The former are likely at risk of developing milk-alkali syndrome. Calcium absorption is completed within 4 hours of intake. Avid absorption of large doses may lead to suppression

2014 eMedicine.com

111. Metabolic Alkalosis (Overview)

tract. Vomiting or nasogastric (NG) suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Whenever a hydrogen ion is excreted, a bicarbonate ion is gained in the extracellular space. Renal losses of hydrogen ions occur whenever the distal delivery of sodium increases in the presence of excess aldosterone, which stimulates the electrogenic epithelial sodium channel (ENaC) in the collecting duct. As this channel reabsorbs sodium ions (...) , the tubular lumen becomes more negative, leading to the secretion of hydrogen ions and potassium ions into the lumen. Shift of hydrogen ions into the intracellular space mainly develops with hypokalemia. As the extracellular potassium concentration decreases, potassium ions move out of the cells. To maintain neutrality, hydrogen ions move into the intracellular space. Administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate may cause

2014 eMedicine.com

112. Metabolic Acidosis (Treatment)

and well tolerated, and was associated with improvements in bone quality, suggesting a beneficial effect of both alkali treatment and restoration of acid/base balance. The researchers concluded that potassium citrate may be superior to sodium bicarbonate, because it lacks volume effects and the obligatory calcium excretion associated with sodium administration. [ ] Go to and for complete information on these topics. Next: Type 1 Renal Tubular Acidosis Administration of an alkali is the mainstay (...) with placebo followed by escalating doses of oral sodium bicarbonate at 2-week intervals (0.3, 0.6, and 1.0 mEq/d per kg ideal body weight). [ ] Sodium bicarbonate was well tolerated, even at high doses; produced a dose-dependent increase in serum bicarbonate; and was associated with an improvement in lower extremity muscle strength and reduced urinary nitrogen excretion. The authors caution, however, that the results require further study and confirmation from a large randomized placebo-controlled study

2014 eMedicine.com

113. Cystinuria (Treatment)

range of 7-7.5. Acetazolamide inhibits the brush-border carbonic anhydrase of the proximal convoluted tubule, thereby increasing urinary bicarbonate excretion. Acetazolamide is not widely used as a first-line drug and is of questionable efficacy. Sodium bicarbonate was used in the past for alkalinizatoinbut is no longer recommended as a first-line agent. The sodium ion may actually increase the amount of cystine excreted. Chelating agents Cystine-binding and cystine-reducing agents share the ability (...) is important for decision-making processes, and stone site and size also influence further management. See the treatment algorithm image below. Treatment algorithm for cystinuria. Hydration The average homozygous patient with cystinuria excretes 600-1400 mg of cystine per day. The solubility of cystine at a pH level of 7 is 250-300 mg/L. Therefore, one of the oldest and most effective cystine stone–prevention techniques is hyperdiuresis to decrease urinary cystine concentration. Early studies by Dent et al

2014 eMedicine.com

114. Acute Tubular Necrosis (Overview)

From ATN Finding Prerenal Azotemia ATN and/or Intrinsic Renal Disease Urine osmolarity (mOsm/kg) >500 < 350 Urine sodium (mmol/d) < 20 >40 Fractional excretion of sodium (FENa) (%) < 1 >2 Fractional excretion of urea (%) < 35 >50 Urine sediment Bland and/or nonspecific May show muddy brown granular casts Contributor Information and Disclosures Author Nikhil A Shah, MBBS, DNB(Neph) Clinical Research Fellow in Home Dialysis, Nephrologist, University of Alberta Faculty of Medicine and Dentistry (...) , but it also helps in the excretion of these toxins by glomerular filtration and tubular secretion. Exogenous nephrotoxins that cause ATN Aminoglycoside-related toxicity occurs in 10-30% of patients receiving aminoglycosides, even when blood levels are in apparently therapeutic ranges. Risk factors for ATN in these patients include the following: Preexisting liver or renal disease Concomitant use of other nephrotoxins (eg, amphotericin B, radiocontrast media, cisplatin) Shock Advanced age Female sex Higher

2014 eMedicine.com

115. Metabolic Acidosis (Follow-up)

and well tolerated, and was associated with improvements in bone quality, suggesting a beneficial effect of both alkali treatment and restoration of acid/base balance. The researchers concluded that potassium citrate may be superior to sodium bicarbonate, because it lacks volume effects and the obligatory calcium excretion associated with sodium administration. [ ] Go to and for complete information on these topics. Next: Type 1 Renal Tubular Acidosis Administration of an alkali is the mainstay (...) with placebo followed by escalating doses of oral sodium bicarbonate at 2-week intervals (0.3, 0.6, and 1.0 mEq/d per kg ideal body weight). [ ] Sodium bicarbonate was well tolerated, even at high doses; produced a dose-dependent increase in serum bicarbonate; and was associated with an improvement in lower extremity muscle strength and reduced urinary nitrogen excretion. The authors caution, however, that the results require further study and confirmation from a large randomized placebo-controlled study

2014 eMedicine.com

116. Hypocitraturia (Follow-up)

filtration rate (GFR) decreases, there is a stepwise decrease in the amount of citrate that is filtered; however, in the early stages of CKD, the increased fractional excretion of citrate prevents an abrupt decline in urinary citrate, such that overt hypocitraturia is not usually observed until advanced stages of CKD. [ ] Primary Hyperaldosteronism In this disease entity, both hypercalciuria and hypocitraturia occur via Na-dependent volume expansion and chronic hypokalemia. [ ] Previous Next: US (...) . Urol Res . 2006 Aug. 34(4):231-8. . Kessler T, Hesse A. Cross-over study of the influence of bicarbonate-rich mineral water on urinary composition in comparison with sodium potassium citrate in healthy male subjects. Br J Nutr . 2000 Dec. 84(6):865-71. . Pinheiro VB, Baxmann AC, Tiselius HG, Heilberg IP. The effect of sodium bicarbonate upon urinary citrate excretion in calcium stone formers. Urology . 2013 Jul. 82(1):33-7. . Seltzer MA, Low RK, McDonald M. Dietary manipulation with lemonade

2014 eMedicine.com

117. Cystinuria (Follow-up)

range of 7-7.5. Acetazolamide inhibits the brush-border carbonic anhydrase of the proximal convoluted tubule, thereby increasing urinary bicarbonate excretion. Acetazolamide is not widely used as a first-line drug and is of questionable efficacy. Sodium bicarbonate was used in the past for alkalinizatoinbut is no longer recommended as a first-line agent. The sodium ion may actually increase the amount of cystine excreted. Chelating agents Cystine-binding and cystine-reducing agents share the ability (...) is important for decision-making processes, and stone site and size also influence further management. See the treatment algorithm image below. Treatment algorithm for cystinuria. Hydration The average homozygous patient with cystinuria excretes 600-1400 mg of cystine per day. The solubility of cystine at a pH level of 7 is 250-300 mg/L. Therefore, one of the oldest and most effective cystine stone–prevention techniques is hyperdiuresis to decrease urinary cystine concentration. Early studies by Dent et al

2014 eMedicine.com

118. Hypertension (Follow-up)

[ , ] : (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg. In adults at increased risk of heart failure (HF), the optimal BP in those with hypertension should be less than 130/80 mm Hg. Adults with HFrEF (HF with reduced ejection fraction) and hypertension should be prescribed GDMT (guideline-directed management and therapy) titrated to attain

2014 eMedicine.com

119. Syndrome of Inappropriate Antidiuretic Hormone Secretion (Diagnosis)

, the nonphysiological secretion of AVP results in enhanced water reabsorption, leading to dilutional hyponatremia. While a large fraction of this water is intracellular, the extracellular fraction causes volume expansion. Volume receptors are activated and natriuretic peptides are secreted, which causes natriuresis and some degree of accompanying potassium excretion (kaliuresis). Eventually, a steady state is reached and the amount of Na + excreted in the urine matches Na intake. Ingestion of water is an essential (...) of the antidiuretic hormone arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion. [ ] The key to understanding the pathophysiology, signs, symptoms, and treatment of SIADH is the awareness that the results from an excess of water rather than a deficiency of sodium. Signs and symptoms Depending on the magnitude and rate of development, hyponatremia may or may not cause symptoms. The history should take into account the following considerations: In general

2014 eMedicine Pediatrics

120. Oliguria (Follow-up)

, and an estimation of fluid status is a prerequisite for initial and ongoing therapy. This is accomplished by determination of input and output, body weights, vital signs, skin turgor, capillary refill, peripheral edema, cardiopulmonary examination, serum sodium, and fractional excretion of sodium (FENa). Children with intravascular volume depletion require prompt and vigorous fluid resuscitation. Initial therapy includes isotonic sodium chloride or lactated Ringer solution at 20mL/kg over 30 minutes, which can (...) < 7.2), especially in the presence of hyperkalemia, requires IV bicarbonate therapy. Recognize that bicarbonate therapy requires adequate ventilation (to excrete the carbon dioxide produced) to be effective, and it may precipitate hypocalcemia and hypernatremia. Patients who cannot tolerate a large sodium load (eg, those with congestive heart failure) may be treated in an ICU setting with IV tromethamine (THAM), with provision of adequate ventilatory support pending institution of dialysis. Previous

2014 eMedicine Pediatrics

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