FUNDAMENTALS OF FLUID AND ELECTROLYTE BALANCE
FLUID REQUIREMENTS Sources
Losses
Water
1500 ml
Urine
1500 ml
Food
800 ml
Stool
200 ml
Oxidation
300 ml
Skin
500 ml
Resp. Tract
400 ml
Total
2600 ml
Total
2600 ml
FLUID CONTENT OF THE BODY
Varies with age, sex, adipose tissue Females 45-50% TBW Males 50-60% TBW Infants 77% TBW
BODY FLUID COMPARTMENTS
RULE Intracellular: Extracellular:
OF THIRDS 2/3 (40% TBW) 1/3 (20% TBW)
a. Interstitial + Lymph: 2/3 (15% TBW) b. Intravascular: 1/3 (5% TBW)
ELECTROLYTES IN BODY FLUID COMPARTMENTS INTRACELLULAR
EXTRACELLULAR
POTASSIUM
SODIUM
MAGNESIUM
CHLORIDE
PHOSPHOROUS
BICARBONATE
IV FLUID DISTRIBUTION IN BODY COMPARTMENTS
Dextrose 5% in Water 1000 ml Sodium Chloride 0.9% 1000 ml
ICF
ECF
2/3 667 ml
1/3 333 ml
1000 ml
SOLUTES
Non-electrolytes • Dextrose • Urea • Creatinine
Electrolytes • Anions • Cations
MAINTENANCE vs. REPLACEMENT
Maintenance: • Provide normal daily requirements: Water: 2.5 L Sodium ½ or ¼ NS KCl 40-60 meq/L
Example: D5 ½ NS with KCL 20 meq/L running at 100 ml/hr
MAINTENANCE vs. REPLACEMENT
Replacement: • Replace abnormal losses with a fluid and electrolytes similar to that which was lost.
OSMOLALITY Definition: Concentration of particles (osmotically active) in solution. It is usually expressed in millosmoles of solute per kg of solution.
Osmolality is independant of valence. Osmolality (mOsm/Kg) of dilute solutions approximate osmolarity (mOsm/L) Plasma: 280-300 mOsm/Kg Same in all body compartments Water distribution
Normal Laboratory Values Sodium Potassium Chloride Bicarbonate Calcium Phosphate Glucose BUN Creatinine Osmolality (P) Osmolality (U)
135-145 meq/L 3.5-5.0 meq/L 95-105 meq/L 22-28 meq/L 9-11 mg/dL 3.2-4.3 mg/dL 70-110 mg/dL 8-18 mg/dL 0.6-1.2 mg/dL 280-295 mOsm/kg 50-1200 mOsm/kg
ELECTROLYE DISORDERS SODIUM JO is a 58 year-old male with cirrhosis of the liver due to ethanol abuse. Physical examination reveal ascites. Baseline lab is as follows: Na 128, K 3.8, Cl 95, CO2 24 JO is to be started on TPN, Should we request additional sodium to correct his hyponatremia?
ELECTROLYE DISORDERS SODIUM
Primary extracellular cation Hyponatremia 1. 2.
Excess of TB water Decrease in TB sodium a. Isotonic hyponatremia (factitious) b. Hypertonic hyponatremia (dilutional)
ELECTROLYTE DISORDERS Hypotonic Hyponatremia Increased ECV
Decreased ECV
Normal ECV
Edematous states
Hypovolemic states
SIADH
CHF Cirrhosis Renal dz Excess of TB Na and water
Diuretic induced GI losses
Sydrome of inappropriate antidiuretic hormone
Depletion of water and Na
Excess of water: dilutional
Treatment: Water and Na replacement Diuretics Water & Na restriction CHF- cardiac glycosides
Fluid restriction Furosemide and NS Chronic: Declomycin
ELECTROLYE DISORDERS SODIUM JO is a 58 year-old male with cirrhosis of the liver due to ethanol abuse. Physical examination reveal ascites. Baseline lab is as follows: Na 128, K 3.8, Cl 95, CO2 24 JO is to be started on TPN, Should we request additional sodium to correct his hyponatremia? JO’s is in an edematous state. He has an excess of TB water and sodium. The appropriate treatment is water and sodium restriction. He should also receive diuretic treatment. The drug of choice is Aldactone (spironolactone), an Aldosterone antagonist.
ELECTROLYE DISORDERS Model for Distribution and Elimination of Intracellular Ions Intake
K
Phos
Mg
ICF
ECF
Renal Losses
Stomach Intestine
GI (stool) Losses
ELECTROLYE DISORDERS POTASSIUM
Primary intracellular cation Hypokalemia: Causes 1. 2.
Decreased dietary intake Redistribution Insulin Metabolic Alkalosis Dehydration
ELECTROLYE DISORDERS POTASSIUM Metabolic Alkalosis and Hypokalemia
Intracellular Fluid
H+
Extracellular Fluid
K+
ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Causes 1. Increased Urinary or GI Losses Diuretics NG Suction Diarrhea
ELECTROLYE DISORDERS POTASSIUM Drugs which may cause hypokalemia Urinary wasting: aminoglycosides, amphotericin B, corticosteroids, diuretics, levodopa, nifedipine, penicillins, rifampin Gastrointestinal losses: laxatives Redistribution: Beta-2 agonists, lithium
ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Treatment/Estimation of Deficit
If serum K > 3meq/L: 100-200 meq required per each change in serum K of 1 meq/L If serum K < 3 meq/L: 200-400 meq required per each change in serum K of 1 meq/L
ELECTROLYE DISORDERS POTASSIUM Hypokalemia: Estimation of Deficit If serum K > 3meq/L: 100-200 meq required per each change in serum K of 1 meq/L If serum K < 3 meq/L: 200-400 meq required per each change in serum K of 1 meq/L
Example: Serum K = 2.5 How much K is required to correct serum K to 4.0? Step 1 To increase from 2.5 to 3.0: 200-400 meq X 0.5=100-200meq Step 2 To increase from 3.0 to 4.0: 100-200 meq X 1.0=100-200meqTo Total=200-400meq
ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Treatment Serum K
Max Infusion Rate
Max. Conc.
Max. Dose 24 hrs
> 2.5meq/L 10 meq/hr
40 meq/L
200 meq
<2meq/L
80 meq/L
400 meq
40 meq/hr
ELECTROLYE DISORDERS POTASSIUM Mrs. D. is a 62 year-old female who is having an acute exacerbation of Crohn’s disease. She complains to you of severe and frequent diarrhea over the last four days. She experiences dizziness when she stands. Your physical examination reveals dry mucous membranes. In the supine position her BP=110/65 and in the upright position her BP=90/45 and her pulse=140. Your lab values are as follows: Na 132, K 2.9, Cl 92, CO2 31, BUN 25, Cr 1.0 Discuss Mrs. D’s fluid and electrolyte problems.
ELECTROLYE DISORDERS Case Study: Hypokalemia Mrs. D. is a 62 year-old female who is having an acute exacerbation of Crohn’s disease. She complains to you of severe and frequent diarrhea over the last four days. She experiences dizziness when she stands. Your physical examination reveals dry mucous membranes. In the supine position her BP=110/65 and in the upright position her BP=90/45 and her pulse=140. Your lab values are as follows: Na 132, K 2.9, Cl 92, CO2 31, BUN 25, Cr 1.0 Mrs. D’s has extracellular volume depletion due to prolonged diarrhea. The ECVD is supported by her physical assessment and postural hypotension and her BUN/Cr is > 20:1. The diarrhea has resulted in a loss of fluid and sodium chloride. Some potassium was lost directly in the stools, but the main cause of her hypokalemia is her ECVD which has induced a metabolic alkalosis (contraction alkalosis.) The alkalosis contributed to her hypokalemia by two mechanisms. Some potassium has moved to the intracellular compartment but much of it has been lost in the urine where potassium wasting occurs secondary to chloride deficit. Administration of Normal Saline with Potassium Chloride will correct her fluid and electrolyte problems (and alkalosis.)
ELECTROLYE DISORDERS POTASSIUM 2.
Hyperkalemia: Causes Decreased Renal Excretion CRF and ARF Drug induced: K-sparing diuretics (Spironolactone, Triamterine, Amiloride) Angiotensin Converting Enzyme inhibitors NSAIDS
ELECTROLYE DISORDERS POTASSIUM 2.
Hyperkalemia: Causes Redistribution Trauma, burns Acidosis Hyperosmolar states
3.
Increased intake Salt substitutes Blood transfusions K salts of antibiotics
ELECTROLYE DISORDERS POTASSIUM Metabolic Acidosis and Hyperkalemia
Intracellular Fluid
K+
Extracellular Fluid
H+
ELECTROLYE DISORDERS POTASSIUM 2.
Hyperkalemia: Treatment Potassium Antagonist Calcium Chloride
3.
Redistribution a. b.
4.
Insulin + Dextrose Sodium Bicarbonate
Cationic Binding Resins Kayexalate (Polystyrene Sulfonate)
6.
Renal Elimination/Dialysis
ELECTROLYE DISORDERS MAGNESIUM 2.
Hypomagnesemia: Causes Decreased Intake Malnutrition Alcoholism
3. 4.
Decreased Absorption Increased Losses GI losses Renal losses
ELECTROLYE DISORDERS MAGNESIUM 2.
Drug Induced Hypomagnesemia GI Losses Laxatives
3.
Renal Losses Diuretics, Cisplatin, Aminoglycosides, Amphotericin B
ELECTROLYE DISORDERS MAGNESIUM 2.
Hypomagnesemia: Treatment IV Magnesium Sulfate Replace over several days Renal threshold for reabsorption of Mg 1 mEq/kg on day 1 0.5 mEq/kg on days x 3-5 days
3.
Oral replacement Mylanta
ELECTROLYE DISORDERS MAGNESIUM
Hypermagnesemia: Causes 1. Exogenous ingestion 2. Impaired renal excretion
Treatment: Eliminate exogenous source of Mg
ELECTROLYE DISORDERS PHOSPHOROUS
Hypophosphatmeia: Causes 1. Impaired absorption Aluminum or calcium binding
2. Redistribution Respiratory alkalosis Glucose + insulin
3. Increased Excretion
ELECTROLYE DISORDERS PHOSPHOROUS
Hyperphosphatmeia: Causes 1. Renal impairment 2. Increased intake
Treatment Phosphate binders: Alternagel, Amphojel, Calcium Supplements
ELECTROLYE DISORDERS PHOSPHOROUS M.T. is a 55 year-old female with a history of chronic renal failure who is admitted to the SICU following a motor vehicle accident. She is started on a TPN solution with minimal K, no Mg and no Phos. She also receives Mylanta II 30 ml per NG tube every four hours. Although her baseline labs were normal on day six her labs are as follows: K 4.3, Mg 2.6, Phos 1.6 5. 6.
What role did the antacid play in her electrolyte abnormalities? What role did the TPN play?
ELECTROLYE DISORDERS PHOSPHOROUS M.T. is a 55 year-old female with a history of chronic renal failure who is admitted to the SICU following a motor vehicle accident. She is started on a TPN solution with minimal K, no Mg and no Phos. She also receives Mylanta II 30 ml per NG tube every four hours. Although her basline labs were normal on day six her labs are as follows: K 4.3, Mg 2.6, Phos 1.6 M.T’s K is normal, but she has hypermagnesemia and hypophosphatemia. The antacid contributed to both of these abnormalities. It provided a significant source of Mg this patient with impaired excretion. Also the aluminum in the antacid acted a phosphate binder contributing to the hypophosphatemia. The TPN could have contributed to the hypophosphatemia by inducing an intracellular shift of phosphate (refeeding). The potassium probably remained normal because some was being provided. Mg was being provided enterally.