1. FUNDAMENTALS OF FLUID AND ELECTROLYTE BALANCE

3. FLUID REQUIREMENTS Sources Losses Water 1500 ml Urine Food 800 ml
Stool
200 ml
Oxidation
300 ml
Skin
500 ml
Resp. Tract
400 ml
Total
2600 ml

4. FLUID CONTENT OF THE BODY
Varies with age, sex, adipose tissue
Females 45-50% TBW
Males % TBW
Infants 77% TBW

5. BODY FLUID COMPARTMENTS
RULE OF THIRDS
Intracellular: 2/ (40% TBW)
Extracellular: 1/ (20% TBW)
Interstitial + Lymph: 2/3 (15% TBW)
Intravascular: /3 (5% TBW)

6. ELECTROLYTES IN BODY FLUID COMPARTMENTS
INTRACELLULAR
EXTRACELLULAR
POTASSIUM
SODIUM
MAGNESIUM
CHLORIDE
PHOSPHOROUS
BICARBONATE

7. IV FLUID DISTRIBUTION IN BODY COMPARTMENTS
ICF
ECF
Dextrose 5% in Water
1000 ml
2/3
667 ml
1/3
333 ml
Sodium Chloride 0.9% 1000 ml

8. SOLUTES Non-electrolytes Electrolytes Dextrose Urea Creatinine Anions
Cations

9. MAINTENANCE vs. REPLACEMENT
Provide normal daily requirements: Water: 2.5 L
Sodium ½ or ¼ NS
KCl meq/L
Example:
D5 ½ NS with KCL 20 meq/L running at 100 ml/hr

10. MAINTENANCE vs. REPLACEMENT
Replace abnormal losses with a fluid and electrolytes similar to that which was lost.

13. OSMOLALITY Osmolality is independant of valence.
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: mOsm/Kg
Same in all body compartments
Water distribution

14. Normal Laboratory Values
Sodium meq/L
Potassium meq/L
Chloride meq/L
Bicarbonate meq/L
Calcium mg/dL
Phosphate mg/dL
Glucose mg/dL
BUN mg/dL
Creatinine mg/dL
Osmolality (P) mOsm/kg
Osmolality (U) mOsm/kg

17. 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?

18. ELECTROLYE DISORDERS SODIUM
Primary extracellular cation
Hyponatremia
Excess of TB water
Decrease in TB sodium
Isotonic hyponatremia (factitious)
Hypertonic hyponatremia (dilutional)

19. 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:
Diuretics
Water & Na restriction
CHF- cardiac glycosides
Water and Na replacement
Fluid restriction
Furosemide and NS
Chronic: Declomycin

20. 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.

21. ELECTROLYE DISORDERS Model for Distribution and Elimination of Intracellular Ions
Intake
K Phos Mg
ICF
ECF
Stomach
Intestine
Renal
Losses
GI (stool)
Losses

22. ELECTROLYE DISORDERS POTASSIUM
Primary intacellular cation
Hypokalemia: Causes
Decreased dietary intake
Redistribution
Insulin
Metabolic Alkalosis
Dehydration

23. ELECTROLYE DISORDERS POTASSIUM Metabolic Alkalosis and Hypokalemia
Intracellular Fluid H+
Extracellular
Fluid K+

24. ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Causes
Increased Urinary or GI Losses
Diuretics
NG Suction
Diarrhea

25. 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

26. ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Treatment/Estimation of Deficit
If serum K > 3meq/L:
meq required per each change in serum K of 1 meq/L
If serum K < 3 meq/L:
meq required per each change in serum K of 1 meq/L

27. ELECTROLYE DISORDERS POTASSIUM
Hypokalemia: Estimation of Deficit
If serum K > 3meq/L:
meq required per each change in serum K of 1 meq/L
If serum K < 3 meq/L:
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: meq X 0.5= meq
Step 2
To increase from 3.0 to 4.0: meq X 1.0= meqTo
Total= meq

28. 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
40 meq/hr
80 meq/L
400 meq

29. 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.

30. 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.)

31. ELECTROLYE DISORDERS POTASSIUM
Hyperkalemia: Causes
Decreased Renal Excretion
CRF and ARF
Drug induced:
K-sparing diuretics (spironolactone, triamterine, amiloride)
Angiotensin converting enzyme inhibitors
NSAIDS

32. ELECTROLYE DISORDERS POTASSIUM
Hyperkalemia: Causes
Redistribution
Trauma, burns
Acidosis
Hyperosmolar states
Increased intake
Salt substitutes
Blood transfusions
K salts of antibiotics

33. ELECTROLYE DISORDERS POTASSIUM Metabolic Acidosis and Hyperkalemia
Intracellular Fluid K+
Extracellular
Fluid H+

34. ELECTROLYE DISORDERS POTASSIUM
Hyperkalemia: Treatment
Potassium Antagonist
Calcium Chloride
Redistribution
Insulin + dextrose
Sodium bicarbonate
Cationic binding resins
Kayexalate (polystyrene sulfonate)
Renal Elimination/dialysis

35. ELECTROLYE DISORDERS MAGNESIUM
Hypomagnesemia: Causes
Decreased Intake
Malnutrition
Alcoholism
Decreased Absorption
Increased Losses
GI losses
Renal losses

36. ELECTROLYE DISORDERS MAGNESIUM
Drug Induced Hypomagnesemia
GI Losses
Laxatives
Renal Losses
Diuretics, cisplatin, aminoglycosides, amphotericin B

37. ELECTROLYE DISORDERS MAGNESIUM
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
Oral replacement
Mylanta

38. ELECTROLYE DISORDERS MAGNESIUM
Hypermagnesemia: Causes
Exogenous ingestion
Impaired renal excretion
Treatment: Eliminate exogenous source of Mg

39. ELECTROLYE DISORDERS PHOSPHOROUS
Hypophosphatmeia: Causes
Impaired absorption
Aluminum or calcium binding
Redistribution
Respiratory alkalosis
Glucose + insulin
Increased Excretion

40. ELECTROLYE DISORDERS PHOSPHOROUS
Hyperphosphatmeia: Causes
Renal impairment
Increased intake
Treatment
Phosphate binders: Alternagel, Amphojel, Calcium Suppliments

41. 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
What role did the antacid play in her electrolyte abnormalities?
What role did the TPN play?

42. 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.