Fundamentals Fluid Electrolyte Balance

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)

Biomedical Importance of Water 

Homeostasis (CES) • Water distribution • PH maintenance • Maintain Electrolyte Concentration



Set of Fluid Balance • Depletion (dehydration) • Intoxication (over-hydration) • Osmotic & non osmotic mechanism

Water as ideal biologic solvent    

   

Tetrahedron structure Bipolar molecule Multiple energy Hydrogen bond determines macromolecule structure The best nucleofil Minor Dissociation Electrostatic interaction Interaction with biomolecule

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. Excess of TB water 2. 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

Diuretic induced GI losses

Sydrome of inappropriate antidiuretic hormone

Excess of TB Na and water

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 intacellular cation Hypokalemia: Causes 1. Decreased dietary intake 2. Redistribution Insulin Metabolic Alkalosis Dehydration

ELECTROLYE DISORDERS POTASSIUM Metabolic Alkalosis and Hypokalemia

Extracellular Fluid Intracellular Fluid

H+

K+

ELECTROLYE DISORDERS POTASSIUM  

Primary intacellular cation Hypokalemia: Causes 1. Increased Urinary or GI Losses Diuretics NG Suction Diarrhea

ELECTROLYE DISORDERS POTASSIUM 

Hypokalemia: Causes 1. Increased Urinary or GI Losses NG Suction Diarrhea Drugs

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

Extracellular Fluid Intracellular Fluid

K+

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 Suppliments

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 5. 6.

What role did the abnormalities? What role did the

antacid play in her electrolyte 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.