Editors: Susla, Gregory M.; Suffredini, Anthony F.; McAreavey, Dorothea; Solomon, Michael A.; Hoffman, William D.; Nyquist, Paul; Ognibene, Frederick P.; Shelhamer, James H.; Masur, Henry
Title: Handbook of Critical Care Drug Therapy, 3rd Edition
> Table of Contents > Chapter 5 - Renal, Electrolyte, and Acid Base Disturbances
Chapter 5
Renal, Electrolyte, and Acid Base Disturbances

TABLE 5.1. Hypernatremia
Therapy Dosage Comments
5% dextrose in water (D5W) or 0.45% NaCl By calculation: see comment Free water replacement is based on formula for calculating water deficit:
Water deficit (L) = normal total body water - estimated total body water
Water deficit = (0.5 × body weight [kg]) - [(0.5 × body weight [kg]) × (140/actual serum Na+)]
Replace half of water deficit in the first 24 h and the remainder over the following 2–3 d
Monitor serum Na+ q1–2h to ensure gradual correction
Correcting too rapidly may produce cerebral edema, seizures, and death
Desmopressin (DDAVP) Intranasal: 0.1–0.4 ml (10–40 µg) qd Can be administered as a single daily dose or divided into 2 doses
  SC/IV: 0.5–1 ml (2.0–4.0 µg) qd When switching from the intranasal to IV route, the comparable antidiuretic dose is approximately 1/10 of the intranasal dose
Vasopressin SC/IM: 5–10 U bid-tid Low cost; however, complications include hypertension and sterile abscesses
IV administration not usually recommended
IM, intramuscular; IV, intravenous; SC, subcutaneous
  • Homeostasis of extracellular fluid is more dominant mechanism than maintenance of osmolality. Hypernatremia may be associated with low, normal, or excessive body water.
  • If thirst mechanism is intact, vasopressin replacement is a matter of convenience.
  • Excessive or rapid correction is particularly dangerous if hypernatremia has persisted for more than 24 hours because there is increased central nervous system intracellular osmolality. In this setting, secondary cerebral edema may produce seizures or death.
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TABLE 5.2. Hyponatremia
Therapy Dosage Comments
Furosemide 20–200 mg IV q4–6h Treatment usually required if serum sodium <110 mEq/L or patient is symptomatic
    Aim to bring serum sodium up to 120–125 mEq/L, but raise no more than 12 mEq/L in the first 24 h
0.9% NaCl (154 mEq Na+/L) By calculation (see comment) Calculation: Na+ deficit (mEq) = 0.60 × lean body wt (kg) × (120 - measured Na+)
3% NaCl (513 mEq Na+/L) By calculation (see comment above) Only for severe neurologic derangements or seizures
Administer very cautiously as overly rapid correction can cause CNS toxicity (central pontine myelinolysis) or volume overload
Demeclocycline 300 mg PO q12h For patients with SIADH
    Antagonizes ADH action in the distal nephron
ADH, antidiuretic hormone; CNS, central nervous system; PO, by mouth; SIADH, syndrome of inappropriate antidiuretic hormone release
  • Important to exclude “spurious” hyponatremia caused by hyperglycemia. This occurs because the osmotically active solute, glucose, causes a shift of water from the intracellular compart- ment to the extracellular compartment and dilutes extracellular sodium. For every 62 mg/dl rise in glucose, there is a 1 mEq/L fall in sodium.
  • The rate of correction of hyponatremia should be proportional to its rate of occurrence. Acute correction of hyponatremia should not exceed a 20 mEq/L rise in concentration of serum sodium in the first 48 hours of therapy.
  • Osmolality (mOsm/kg) = 2(Na+ + K+) + (BUN/2.8) + (glucose/18).
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TABLE 5.3. Hyperkalemia
Therapy Dosage Onset/Duration Comments
Acute Management
Sodium bicarbonate (NaHCO3) 1 mEq/kg IV over 3–5 min Onset: 15–30 minDuration: 1–2 h Can cause sodium overload and hyperosmolality
Calcium gluconate 10% (100 mg/ml = 9 mg/ml elemental Ca+2, 0.46 mEq/ml) 5–10 ml IV over 2–5 min Onset: 1–5 min
Duration: 1–2 h
Rapid onset, but short-lived
Not compatible with NaHCO3; must flush line between infusions
Can augment digoxin toxicity
Calcium chloride 10% (100 mg/ml = 27.2 mg/ml elemental Ca+2, 1.36 mEq/ml) 5–10 ml IV over 2–5 min Onset: 1–5 min
Duration: 1–2 h
Rapid onset, but short-lived
Not compatible with NaHCO3; must flush line between infusions
Can augment digoxin toxicity
Preferred preparation when volume is an issue because it contains more elemental calcium per g than calcium gluconate
Dextrose and insulin Dextrose 0.5 g/kg with 0.3 U regular insulin per g dextrose Onset: 10–15 min
Duration: 3 h
Usual dosing is 25 g dextrose with 6–10 U regular insulin
Insulin should be given IV to avoid delayed hypoglycemia that can follow SC insulin; important to administer glucose concurrently
Albuterol 10–20 mg via nebulized aerosol Onset: 30 min
Duration: 2 h
Mechanism is intracellular shunting of potassium by β 2-adrenergic agonists
Beware of possible angina
Subacute and Chronic Management
Sodium polystyrene sulfonate (SPS) PO: 15–60 g in 100–200 ml 20% sorbitol q4h
PR: 50 g in 50 ml 70% sorbitol added to 100–200 ml water
Onset:
PO: 2 h
PR: 1 h
Duration: 4 h
Resin exchanges sodium for potassium in the gut
PO SPS removes 1 mEq KCl/g, PR SPS removes 0.5 mEq KCl/g
Be aware of sodium load in patients with heart failure
IV, intravenous; PO, by mouth; PR, per rectum; SC, subcutaneous
If conservative methods of therapy fail, up to 50 mEq/h of potassium can be removed by hemodialysis. Peritoneal dialysis removes approximately 10 mEq/h.
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TABLE 5.4. Hypokalemia
Therapy Dosage Comments
Potassium chloride (KCl) See sliding scale for IV infusion (Table 5.5)
Maximum infusion rate of 40 mEq/h IV through a central line with continuous cardiac monitoring
Solutions should be prepared in non-dextrose containing fluids (i.e., NS or 0.45% NaCl)
Life-threatening hypokalemia usually is caused by gastrointestinal losses (diarrhea) or genitourinary losses (diuretics)
Magnitude of deficit can only be approximated
Loss of 200–400 mEq of potassium lowers plasma potassium by 1 mEq/L
Clinical manifestations are rare when potassium level is ≥2.5 mEq/L, the exception being patients with cardiac disease
The most serious complications are conduction disturbances and arrhythmias; muscle weakness can occur
Cautious replacement in oliguric or anuric patients
Peripheral IV administration can be painful; pain is less if solutions contain less than 60 mEq KCl/L
Rapid IV replacement (greater than 20 mEq/h) warrants continuous cardiac monitoring
Check magnesium and supplement if below lower limit of normal
Potassium citrate and citric acid 40–60 mEq PO bid to qid Solution of 1,100 mg potassium citrate and 334 mg citric acid monohydrate per 5 ml; equivalent to 2 mEq potassium and 2 mEq bicarbonate per ml
Dose may be adjusted based on urine pH
Useful in renal tubular acidosis, when replacement of both potassium and bicarbonate is required
Aggressive treatment of acidosis with bicarbonate alone may aggravate coexisting hypokalemia
NS, normal saline (0.9%); NaCl, sodium chloride.
Potassium sparing diuretics may be considered in patients with severe renal losses of potassium; however, they should not be used in patients with renal insufficiency or in conjunction with aggressive potassium supplementation.
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TABLE 5.5. Sliding Scale Algorithm for Potassium Chloride (KCl) Infusion
K+ (mEq/L) KCl Infusion Rate (mEq/h)
<2.5 20–40
2.5–3.0 15–20
3.1–3.5 10
3.6–4.0 5
>4.1
Potassium level should be checked frequently—i.e., every 4 to 6 hours, during IV infusion.
Patients receiving ≥15 mEq/h should have cardiac monitoring. Doses ≥15 mEq/h should ideally be delivered via central vein because of pain with peripheral administration. (Maximum recommended concentration is 0.4 mEq/ml of solution.)
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TABLE 5.6. Hypercalcemia
Therapy Dosage Comments
0.9% NaCl 250–500 ml/h With or without furosemide 20 mg IV q4–6h
Volume expansion in patients with normal renal function leads to urinary calcium losses
Calcium loss up to 2 g/24 h
Need to monitor magnesium, phosphorus, and potassium
Calcitonin-salmon Initial: 4 IU/kg SC/IM q12h
Repeat: 8 IU/kg SC/IM q12h
Perform skin test for allergy before first dose in patients with suspected sensitivity to calcitonin-salmon
Decreases bone reabsorption, but effect is limited and diminishes after several days
Maximum dose 8 IU/kg q6h if no response to lower doses
May be added to bisphosphonate to achieve normal calcium levels within a few days
Zoledronic acid 4 mg IV as a single dose over at least 15 min Minimum time period for retreatment is 7 d
Pamidronate disodium 60 mg (for moderate hypercalcemia) or 90 mg (for severe hypercalcemia) as a single IV infusion (diluted in 1 L 0.9% NaCl or D5W) over 24 h Moderate hypercalcemia: corrected serum calcium 12–13.5 mg/dl; severe hypercalcemia: corrected serum calcium >13.5 mg/dl
A minimum of 7 d should elapse to assess response before re-treatment
If retreating, dosage is same as initial dose
Osteonecrosis of the jaw may occur in patients with cancer
Gallium nitrate 100 mg/M2 IV (for mild hypercalcemia), 150 mg/M2 IV (moderate hypercalcemia), or 200 mg/M2 IV (severe hypercalcemia) in 1 L 0.9% NaCl or D5W infused over 24 h × 5 d If serum calcium is lowered to normal range in less than 5 d, treatment may be discontinued
Potential for nephrotoxicity
Hydrocortisone 1 mg/kg IV q8h Especially effective in patients with sarcoidosis, breast carcinoma, and hematologic malignancies
Equivalent doses of other glucocorticoids (dexamethasone or methylprednisolone) may be used (see Table 6.1)
IM, intramuscular; IV, intravenous; SC, subcutaneous
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TABLE 5.7. Hypocalcemia
Therapy Dosage Comments
Acute Therapy
Calcium gluconate 10% (100 mg/ml = 9 mg/ml elemental Ca+2, 0.46 mEq/ml) Initial: 1 g (10 ml) IV over 10 min
Infusion: 100 mg/h
Treat as medical emergency if symptomatic (seizures, confusion, tetany, laryngospasm, arrhythmias, hypotension)
Therapy of acidosis with bicarbonate lowers ionized serum calcium further
Calcium infusion should be continued until elemental calcium level reaches 8–9 mg/dL, then monitor levels and administer as needed
Concomitant magnesium supplementation is often required to maintain calcium level
Calcium chloride 10% (100 mg/ml = 27.2 mg/ml elemental Ca+2, 1.36 mEq/ml) Initial: 1 g (10 ml) IV over 10 min
Infusion: 100 mg/h
Preferred preparation when volume is an issue because it contains more elemental calcium per g than calcium gluconate
Increased bioavailability in hepatic failure
Chronic Therapy
Calcium carbonate 1.25–5 g PO daily in 3–4 divided doses 1.25 g calcium carbonate contains 500 mg elemental calcium
Ergocalciferol (vitamin D2) 25,000 to 150,000 U/d PO Used for the treatment of chronic hypocalcemia, rickets, familial hypophosphatemia, and hypoparathyroidism
Start therapy with oral calcium
Slow acting preparation
Long duration of action; if hypercalcemia develops, it may not resolve for weeks
Inexpensive
Dihydrotachysterol 0.125–1 mg PO qd Used for the treatment of chronic hypocalcemia, acute, chronic and latent forms of postoperative tetany and idiopathic tetany, and hypoparathyroidism
Fast onset; expensive
Calcitriol 0.5–2 µg PO qd Acute hypocalcemia
Rapid onset
If hypercalcemia occurs, it is not long lasting
Calcifediol 50–100 µg PO gd Used for the treatment and management of metabolic bone disease or hypocalcemia in patients on chronic renal dialysis
Intermediate duration of action
Doxercalciferol 10 µg PO 3 times weekly Used for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis
Maximum dose 20 µg 3 times weekly
Intermediate duration of action
Paricalcitol 0.04–1 µg/kg IV every other day during hemodialysis Used for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis
Intermediate duration of action
IV, intravenous; PO, by mouth
  • Clinically significant hypocalcemia is an uncommon problem, but it may occur after multiple rapid transfusions, parathyroidectomy, thyroidectomy, or severe pancreatitis.
  • Correction for calcium in the setting of hypoalbuminemia: total serum calcium will fall 0.8 g/dl for every 1 g decrease in serum albumin.
  • Consider obtaining measurement of ionized calcium to most accurately determine degree of calcium deficit.
  • Calcium preparations should be diluted to prevent phlebitis and to limit tissue necrosis if extravasated.
  • Do not administer calcium in solutions with either bicarbonate or phosphate; insoluble salts can form.
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TABLE 5.8. Hyperphosphatemia
Therapy Dosage Comments
Aluminum hydroxide 30–120 ml PO q4–6h Can cause constipation
Hemodialysis or peritoneal dialysis    
Acetazolamide 15 mg/kg q3–4h  
NS infusion    
NS, normal saline (0.9%); PO, by mouth
Acute, severe hyperphosphatemia in association with symptomatic hypocalcemia can be life threatening. Hyperphosphatemia is associated with tumor lysis, rhabdomyosis, exogenous phosphate administration, lactic, or ketoacidosis.
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TABLE 5.9. Hypophosphatemia
Therapy Dosage Comments
Potassium phosphate (K2PO4) or sodium phosphate (Na2PO4) For mild to moderate hypophosphatemia (PO4 = 1.6–3.0 mg/dL): 0.16–0.32 mmol/kg IV over 6–8 h
For severe hypophosphatemia (PO4 = <1.5 mg/dL): 0.64 mmol/kg IV over 6–8 h
Muscle weakness caused by hypophosphatemia can precipitate or exacerbate heart failure, respiratory failure, and neurologic symptoms
Intravenous replacement warranted for serum phosphate levels less than 1 mg/dl
Be cautious of IV therapy in patients with hypercalcemia because metastatic calcification may occur
Maximum phosphate infusion rate is 10 mmol/h (Ann Pharmacother 1997;31:683)
Important metabolic replacement in hyperalimentation solutions
1 mmol phosphate = 31 mg phosphate
Each ml of potassium phosphate contains phosphate 3 mmol and potassium 4.4 mEq; beware of hyperkalemia and follow potassium levels
Each ml of sodium phosphate contains phosphate 3 mmol and sodium 4 mEq
Potassium and sodium phosphate for oral solution 250–500 mg (8–16 mmol) PO qid Oral therapy is preferred when serum phosphate levels approach 2 mg/dL
May require days to replenish intracellular stores of phosphorus, even after serum levels normalize
Each capsule/packet contains K+ 7 mEq and Na+ 7 mEq
IV, intravenous; PO, by mouth
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TABLE 5.10. Acidosis
Drug Dosage Indications Comments
Sodium bicarbonate (NaHCO3) By calculation (see comment below) Severe nonanion gap metabolic acidosis or hyperkalemia Generally not given unless pH <7.20 or HCO3- <10 mEq/L
Usual rate of administration is 2–5 mEq/h
Can cause chemical phlebitis or cellulitis
Many drug incompatibilities; flush line after use
After cardiac arrest, reversal of acidosis results from adequate ventilation and blood flow. May consider use upon return of spontaneous circulation after long arrest interval (1 mEq/kg IV). Not recommended for routine use after cardiac arrest.
May be associated with paradoxical mixed venous acidosis
Can cause sodium overload and hyperosmolality
Treatment of underlying etiology (i.e., sepsis, hypoperfusion, poisoning) is essential to reverse acidosis
  • Decision to treat is controversial and depends on clinical situation; indications vary with etiology such as bicarbonate responsive acidosis (e.g., diabetic ketoacidosis).
  • Bicarbonate deficit, an approximation of the amount of bicarbonate replacement needed to return bicarbonate concentration to normal:
       HCO3- deficit = body weight (kg) × 0.4 × (desired [HCO3-] - measured [HCO3-])
  • In patients with chronic metabolic acidosis caused by chronic renal failure, replace with bicarbonate when bicarbonate concentration is less than 15 mEq/L to prevent osteomalacia.
  • Treatment of lactic acidosis should be directed to the underlying etiology.
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TABLE 5.11. Alkalosis
Therapy Dosage Indications Comments
Potassium chloride (KCl) Mild alkalosis: 100–150 mEq/d
Severe alkalosis: Up to 300 mEq/d
Chloride-responsive alkalosis Will replete not only chloride, but also potassium deficit, which may be substantial, especially with diuretic-induced alkalosis
Spironolactone or potassium-sparing diuretics may be useful in hypokalemic patients
Sodium chloride (NaCl) Mild alkalosis: 100–150 mEq/d
Severe alkalosis: Up to 300 mEq/d
Chloride-responsive alkalosis Alternative to KCl
Use with caution in patients with HF
Acetazolamide 5 mg/kg qd up to qid (PO/IV) Works well in edematous patients with cirrhosis or HF Carbonic anhydrase inhibitor; impairs renal sodium and renal bicarbonate resorption, thus reducing net acid excretion
Will have diuretic effect and may cause potassium losses
Hydrochloric acid (HCl) 0.1 N HCl by calculation (see comment) For rapid correction of severe metabolic alkalosis Concentration is 100 mEq HCl per 1 L sterile water
Must administer via a central venous line
Amount of H+ needed to correct deficit can be determined by formula: H+ (mEq) = 0.5 × weight (kg) × (103 - serum chloride)
Ammonium chloride By calculation (see comment) Metabolic alkalosis due to significant chloride losses Ammonium ions are converted to urea in the liver with the generation of hydrogen and chloride ions
Should not be given to patients with hepatic failure
H+ (mEq) = 0.5 × weight (kg) × (103 - serum chloride)
HF, heart failure; IV, intravenous; PO, by mouth
Correct volume, potassium, and chloride depletions.
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TABLE 5.12. Tumor Lysis Syndrome
Complication Intervention Comments
Associated with rapidly growing malignancies (eg. leukemias, lymphomas) that are highly chemo or radio sensitive. Therapy initiated before administration of chemotherapy. Syndrome char- acterized by increases in uric acid, potassium, phosphate, and decreases in calcium that may result in renal failure, arrhythmias, seizures, or sudden death.
Pretreatment Evaluation and Preparation
Volume loading and diuresis Hypotonic fluids (D5W/0.45% NaCl) 3,000 ml/M2/day Loop diuretics if necessary to maintain urinary output
Evaluate renal function Monitor weight, intake and output, and electrolytes Ultrasound
Attempt to relieve obstructive uropathy if present
Control uric acid Increase clearance (diuresis), prevent uric acid synthesis, increase degradation Allopurinol 200–400 mg/m2/d IV (max. 600 mg/d) until serum uric acid is normal
Rasburicase 0.15–0.2 mg/kd qd × 5 d
Correct acidosis
Alkalinize urine (pH >7.0) with NaHCO3 (100–150 mEq in 1 L D5W or sterile water) is controversial and may promote Ca2PO4 deposition in the kidney, heart, and other organs if hyperphosphatemia is present
Alkalinization is not required with a uricase
Dialyze if urate nephropathy presents with oliguria
Control phosphate Initiate oral phosphate binders (aluminum hydroxide) if adequate GI function  
Delay chemotherapy if necessary Until good urine output established and uric acid controlled Initiate hemodialysis if indicated; oliguria due to acute uric acid nephropathy is very responsive to dialytic therapy
Postchemotherapy Management
Volume replacement and diuresis Maintain forced diuresis Omit NaHCO3 from IV solutions because of phosphate crystallization in urine
Monitor electrolytes Monitor every 4–6 h depending on tumor burden and/or rate of biochemical changes Monitor ECG for hyperkalemia and/or hypocalcemia
Control uric acid Allopurinol 200–400 mg/M2/day PO for the first 3 d of chemotherapy, then 200 mg/M2/d PO maintenance
Rasburicase 0.15–0.2 mg/kd qd × 5 d
 
Renal failure Hemodialysis Indications:
Oliguria/azotemia
Uncontrolled hyperkalemia
Symptomatic hypocalcemia
Uric acid nephropathy or rapidly rising uric acid
Phosphate nephropathy or rapidly rising phosphate
Iatrogenic volume overload in the face of oliguria
Continuous arterial or venovenous hemofiltration or hemodiafiltration will control volume status but may not maintain rapid efficient clearance of potassium if tumor lysis is overwhelming
ECG, electrocardiogram; GI, gastrointestinal; IV, intravenous; PO, by mouth
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TABLE 5.13. Diuretics
Site of Action Type of Diuresis, Onset, and Duration Usual Dosage Comments
Loop of Henle K+ and Na+ wasting, hypo-osmotic or isosmotic urine   Ototoxicity with bumetanide, furosemide, and torsemide in high doses; clinically effective when GFR <25 ml/min
Bumetanide Onset:
   PO: 30 min
   IV: <10 min
Duration:
   PO: 5–6 h
   IV: 4 h
Bolus:
   0.5–1.0 mg
   q2–3 h prn
Infusion:
   0.08–0.3 mg/h
PO: 0.5–2 mg tid-qd
Bumetanide 1 mg ≈ furosemide 40 mg
Doses >10 mg PO or 20 mg IV may be required in patients with renal failure or in the management of edema or hypertension
IV loading dose may be used before starting infusion
Furosemide Onset:
   PO: 60 min
   IV: 5 min
Duration:
   PO: 6 h
   IV: 2 h
Bolus:
   20–80 mg
   q1–2h prn
Infusion:
   3–12 mg/h
PO:
   20–80 mg
   q6–8h prn
IV doses of 400 mg per bolus or 3–7 g total per day have been used in some patients
IV bolus doses are usually doubled until a maximum dose of 400 mg is reached
An IV loading dose may be used before starting infusion
Furosemide IV dose = 60% to 70% PO dose
Torsemide Onset:
   PO: 60 min
   IV: 15 min
Duration:
   PO: 6–8 h
   IV: 6–8 h
Bolus:
   25 mg
Infusion:
   3–10 mg/h
PO:
   5–40 mg qd
Inject IV dose over 2 min
Dose can be titrated upward by doubling the dose until therapeutic effect achieved or maximum dose of 200 mg is attained, although 400–800 mg may be required in patients with acute renal failure
Torsemide IV dose = PO dose
Torsemide 10–20 mg = furosemide 40 mg = bumetanide 1 mg
Patients with CrCl 15–20 ml/min and HF may require an initial infusion rate of 10 mg/h
IV loading dose may be used before starting an infusion
Distal Tubule ± Proximal Tubule Moderate natriuresis and potassium wasting   May be ineffective when GFR <25 ml/min
Commonly used in combination with loop diuretics to enhance efficacy
Chlorothiazide Onset:
   PO: 60 min
   IV: 15 min
Duration:
   PO: 6–8 h
   IV: 6–8 h
IV bolus or PO: 500–1,000 mg bid-qid  
Hydrochlorothiazide Onset:
   PO: 2 h
Duration:
   PO: 12–18 h
PO: 25–100 mg qd  
Metolazone Onset:
   PO: 1 h
Duration:
   PO: 12–24 h
PO: 5–20 mg qd Thiazide type diuretic
Administer 30 min before IV diuretic
Collecting Duct (Potassium Sparing) Weak diuretics; risk of hyperkalemia is relative contraindication
Triamterene Onset:
   PO: 2–4 h
Duration:
   PO: 12–16 h
PO: 100–200 mg qd Maximum dose 300 mg/d
Amiloride Onset:
   PO: 2 h
Duration:
   PO: 24 h
PO: 5–20 mg qd  
Spironolactone Onset:
   PO: >24 h
Duration:
   PO: 48–72 h
PO: 25–200 mg/d given qd or bid Gradual onset of diuresis with maximal effect on 3rd day
Proximal Tubule
Acetazolamide Onset:
   PO: 30 min
   IV: 5 min
Duration:
   PO: 6–8 h
   IV: 4–5 h
For alkalosis:
   5 mg/kg/d mg IV/PO qid-qd × 2–4 d
For edema:
   5 mg/kg/d IV/PO divided bid-qid
Carbonic anhydrase inhibitor, causes bicarbonaturia and potassium wasting
CrCl, creatinine clearance; GFR, glomerular filtration rate; HF, heart failure; IV, intravenous; PO, by mouth
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TABLE 5.14. Electrolyte Composition of Common IV Solutions
  mEq/L Osm Calories
Na+ Cl- K+ HCO3- Mg+2 Ca+2
Crystalloid
0.9% NaCl (NS) 154 154 292
0.9% NaCl & 5% dextrose in water (D5W/NS) 154 154 565 170
0.45% NaCl (1/2 NS) 77 77 146
0.45% NaCl & 5% dextrose in water (D5W-1/2NS) 77 77 420 170
0.2% NaCl & 5% dextrose (D5W-1/4 NS) 34 34 330 170
5% dextrose in water (D5W) 274 170
10% dextrose in water (D10W) 548 340
Ringer's lactate (RL) 130 109 4 28a 3 277
3% NaCl (hypertonic saline) 513 513 960
Colloid
Hetastarch 6% 154 154 310
Hetastarch 6% in lactated electrolyte injection 143 124 3 28a 9 3 307 340
5% albumin (5 g/100 ml) 145 145    
25% albumin (25 g/100 ml) 145 145    
aPresent in solution as lactate, which is metabolized to bicarbonate (HCO3-).