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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 OF THIRDS
 Intracellular: 2/3 (40% TBW)
 Extracellular: 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

ICF ECF

Dextrose 5% in 2/3 1/3


Water 667 ml 333 ml
1000 ml
Sodium Chloride
0.9% 1000 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 135-145 meq/L
Potassium 3.5-5.0 meq/L
Chloride 95-105 meq/L
Bicarbonate 22-28 meq/L
Calcium 9-11 mg/dL
Phosphate 3.2-4.3 mg/dL
Glucose 70-110 mg/dL
BUN 8-18 mg/dL
Creatinine 0.6-1.2 mg/dL
Osmolality (P) 280-295 mOsm/kg
Osmolality (U) 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 Diuretic induced Sydrome of


Cirrhosis GI losses inappropriate
antidiuretic hormone
Renal dz
Excess of TB Na and Depletion of water Excess of water:
water and Na dilutional

Treatment: Water and Na Fluid restriction


Diuretics replacement Furosemide and NS
Water & Na restriction Chronic: Declomycin
CHF- cardiac
glycosides
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
Stomach
Intestine

Renal GI (stool)
Losses Losses
ELECTROLYE DISORDERS
POTASSIUM
 Primary intracellular cation
 Hypokalemia: Causes
1. Decreased dietary intake
2. Redistribution
Insulin
Metabolic Alkalosis
Dehydration
ELECTROLYE DISORDERS
POTASSIUM
Metabolic Alkalosis and Hypokalemia

Extracellular
Intracellular Fluid
Fluid
K+
H+
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 Max. Max. Dose


Infusion Conc. 24 hrs
Rate
> 2.5meq/L 10 meq/hr 40 meq/L 200 meq

<2meq/L 40 meq/hr 80 meq/L 400 meq


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
 Hyperkalemia: Causes
2. Decreased Renal Excretion
CRF and ARF
Drug induced:
K-sparing diuretics (Spironolactone,
Triamterine, Amiloride)
Angiotensin Converting Enzyme inhibitors
NSAIDS
ELECTROLYE DISORDERS
POTASSIUM
 Hyperkalemia: Causes
2. 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
Intracellular Fluid
Fluid
H+
K+
ELECTROLYE DISORDERS
POTASSIUM
 Hyperkalemia: Treatment
2. Potassium Antagonist
Calcium Chloride
3. Redistribution
a. Insulin + Dextrose
b. Sodium Bicarbonate
4. Cationic Binding Resins
Kayexalate (Polystyrene Sulfonate)
6. Renal Elimination/Dialysis
ELECTROLYE DISORDERS
MAGNESIUM
 Hypomagnesemia: Causes
2. Decreased Intake
Malnutrition
Alcoholism
3. Decreased Absorption
4. Increased Losses
GI losses
Renal losses
ELECTROLYE DISORDERS
MAGNESIUM
 Drug Induced Hypomagnesemia
2. GI Losses
Laxatives
3. Renal Losses
Diuretics, Cisplatin, Aminoglycosides,
Amphotericin B
ELECTROLYE DISORDERS
MAGNESIUM
 Hypomagnesemia: Treatment
2. 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. What role did the antacid play in her electrolyte


abnormalities?
6. 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.

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