FLUIDS AND
ELECTROLYTES
Jacquelyn O’Herrin, MD
University of Colorado
Axioms
Never completely trust the lab
Correct lab abnormalities at the rate at
which they developed
Priorities in treating abnormalities
Restore normal or increased perfusion
Correct pH
Correct K, Ca, Mg
Na and Cl abnormalities are usually corrected
last
Fluid Spaces
Total body water- 50-70% of body
weight
60% in young males
50% in young females
Blood- 7% BW (4900 cc in 70 kg man)
Extracellular fluid - 20% of BW
Interstitial
Plasma
Bone, connective tissue, transcellular
Important Principles
All metabolic processes intracellular
ECF is conduit for transport of O2,
substrate into cell and CO2, metabolites
out of cell
Plasma to ISF equilibration times rapid
ECF to ICF times are slower and variable
Daily Fluid Needs
Basic needs = Urine + Insensible loss
approx. 1500 cc/m2/day
Urine = 0.5-1.0 ml/kg/hr
If max concentrated need 1200 cc/day to clear
600 mOsm solute daily
Insensible H2O loss
600-1000 cc/day from skin
200-400 cc/day from lungs
Daily Fluid Needs
Current losses
Fever - 250-500 cc/day per 1o C fever
Sweating = 500-1500 ml/day = 1/4 N saline
Deficits
Mild, moderate, severe = 6, 8, 10% of BW in
adults
Open peritoneum loses 500-1000 ml/hr H2O
Tissue edema not apparent until 2-4 liters of
extra H2O present
GI Tract Fluids
Saliva
Gastric juice
Bile
Pancreas
Small bowel
Total
400-800 ml/24hrs
1500-2000 ml
500-900 ml
1600-2500 ml
2000-3000 ml
6000-9000 ml
Daily Water Losses
Insensible
Urine
GI
Total
600-800 cc
1000-1600 cc
200-400 cc
1800-2600 cc
Exam Answers...
“When you breathe, you inspire. When you
do not breathe, you expire.”
Tests to Differentiate
Prerenal and Renal
Oliguria
Osmolality
 Calculated serum osmolality
= (2 x
Na)+(glu/18)+(BUN/2.8)
Normal is 285-310 mOsm/L
Measured osmolality is 5-10 mOsm/L higher
than calculated normally
Osmolal gap > 10 is abnormal
Causes of increased gap are ethanol, methanol,
ethylene glycol, acetone, salicylates
Osmolality
Osmoreceptor center
Anterior inferior hypothalamus
ADH formed in post inf hypothalamus
ADH acts on distal tubule to increase
permeability to H2O but not Na
Osmotic shifts
Increased serum osm - increased ADH
release
Decreased serum osm - decreased ADH
release
Dehydration (too little
water)
Mild (4%)
dry skin, urine osm 500-700
Moderate (6%)
above plus dry tongue
dry axillae, groins, urine osm 700-900
Severe (8%)
Above plus soft globe, weakness,
hypotension, lethargy, ileus
urine osm 900-1240
Shock (>8%)
Treatment for Dehydration
Hypoosmolal deficits
vomiting, diarrhea, ileus, severe trauma
LR or NS
Isoosmolal
hyperosmolal non-ketotic dehydration
hypernatremia, osmotic diuresis, hyperglycemia
insulin, control sepsis, rehydration with
D5/0.45NS
Diabetes Insipidus
Increased Na in ECF
Dilute, voluminous urine
D5W or 1/4 NS/D5
Vasopressin or DDAVP
Too much Water
SIADH
Etiology: head trauma, tumor of CNS,
inflammatory CNS disease, paraneoplastic
syndrome (lung, thyroid, breast, adrenal,
sarcoma)
Symptoms: weakness, lethargy, diplopia,
stupor, coma, convulsions, decreased Na,
increased urine osm
Treatment: withhold water, lithium HCO3,
declomycin, furosemide, correct Na deficit
slowly
From patients’ charts...
“ The skin was moist and dry”
Electrolyte Composition
Sodium
Hyponatremia
Increased ECF (most common cause)
Look for excess hypotonic fluid administration
Urine Na > 20 then consider renal failure
Normal ECF
Urine Na > 20 = SIADH, low serum osmolality
Treatment
if ECF excess and no sx then fluid restriction
If ECF excess and sx then diuretic and 3% NaCl
If ECF deficit then saline replacement
Hypernatremia
Etiology: loss of body water, diabetes
insipidus, severe hypokalemia, inadequate
H2O intake
Treatment:
if DI then use DDAVP
if ECF is low then gradual water repletion
use hypotonic solutions cautiously
if ECF is high then diuretics and hypotonic
fluid
Potassium
The major intracellular cation
Required for glucose transport across cell
membrane
Intake = 2 mEq/gm protein=50-100 mEq/day
Losses
paralytic ileus
GI losses
nephropathy or diuretics
bowel prep
Cushing’s disease
Potassium
Hypokalemia
Intracellular shift with alkalosis
0.1 increase in pH = 0.5 mEq/l decrease in K
Reduced intake, esp. protein
Symptoms
ileus (if K < 2.5)
most common cause of paradoxic aciduria
arrhythmias
often associated with Mg and PO4 deficiencies
Hypokalemia
Diagnosis
Correlate K and pH levels
EKG changes- flattened T waves, prominent U
wave
Treatment
Remove cause
Correct alkalosis and stop diuretics
Replace with 10-20 mEq KCl per hour
Check serum values every 4 hours
Hyperkalemia
Etiology
Hemolysis
Acidosis
Increased intake
Oliguric renal failure
GI bleeding, increased tissue destruction
Massive transfusions, electric or crush
injuires
Adrenal insufficiency
Hyperkalemia
Effects
Decreased contractility, conductivity if >6.0
Cardiac blocks if > 6.5
Treatment
Emergency (arrhythmias)
Ca gluconate or chloride
NaHCO3 - give slowly
Insulin + glucose (50 gm glu + 10-20 units insulin over 1
Diuretics
Kayexalate
Dialysis
From patients charts...
“ By the time he was admitted, his rapid
heart stopped, and he was feeling better.”
Calcium
Avg daily intake = 1,000 mg
Avg GI absorption = 300-350 mg
active absorption with Vit D
passive absorption is concentration dependent
300 - 350 mg lost daily thru urine and stool
Calcium in blood in three different forms
Ionized
Protein bound (albumin, globulin)
Complexed (bound to HCO3, PO4)
Hypocalcemia
Etiology
Hypoproteinemia
Fat embolism syndrome
Sepsis, shock
Hypomagnesemia, hypoparathyroidism
Alkalosis
Renal failure, rhabdomyolysis
Pancreatitis
Massive blood transfusions
Hypocalcemia
Effects
Increased DTR’s
Chvostek’s sign
Trousseau’s sign
abdominal cramps
convulsions
Decreased contractility
Increased urine excretion of PO4, HCO3
Hypocalcemia
Treatment:
Correct underlying problem
Ca Gluconate or chloride
Give Ca with blood transfusions if infusion
rate > 1 unit/hr
Chronic therapy requires large doses of Vit D
and elemental Ca
Hypercalcemia
Etiology
Malignancies (most common causeoverall
and in hosp)
Hyperparathyroidism (80-90% single
adenoma)
Immobilization
Thiazides
Hypercalcemia
Effects
Stones (renal)
Bones (lytic lesions)
Moans (psychiatric disorders)
Groans (abd pain with peptic ulcer or
pancreatitis)
Hypokalemia, phosphaturia
Severe dehydration
Hypercalcemia
Diagnosis
Increased ionized Ca
Increased PTH-hyper PTH
Total Ca > 14 then suspect malignancy
Decreased QT interval
Increased PTH think MEN
I = pituitary, panc. Islets, PTH
II a = medullary CA thyroid, pheo, PTH
Hypercalcemia
Treatment
Rehydration with saline
Lasix after correcting dehydration
Prevent hypokalemia
Control primary cause
Mithramycin-suppresses Ca release from
bone
Glucocorticoids for malignant hypercalcemia
Calcitonin blocks bone resorption
“Just the chicken.” - waitresses response
when asked if there were any dairy
products in a soup.
Hypomagnesemia
Etiology
Malnutrition, alcoholism
Diarrhea, vomiting
Renal wasting with diuretics
Hypoparathyroidism, pancreatitis
Effects
muscle irritability, arrhythmias
CNS changes
Hypokalemia, hypocalcemia
Anemia due to shortened RBC survival
Hypomagnesemia
Blood levels may be normal
Signs of hypocalcemia but normal ionized
Ca
EKG changes resemble hypokalemia
Treatment
1-2 gms MgSO4 in first 2-4 hours
total of 6-12 gms in first day for severe
Hypermagnesemia
Etiology
renal failure, severe acidosis, adrenal
insufficiency, severe burns
Effects
lethargy, weakness, somnolence, coma
Diagnosis
Suspect if hyperkalemia, hypercalcemia,
renal failure, loss of DTR
Treatment
Same as hypercalcemia
Hypochloremia
Etiology
Metabolic alkalosis (fall in Cl = 1 1/2 x rise in HCO3)
Excessive diuresis, excess vomiting
Effects- usually due to associated hyponatremia,
hypokalemia
Diagnosis- check urine Cl
< 10-20 = chloride responsive
> 20-40 = chloride resistant
Treatment
Cl responsive- fluids with Cl
Cl resistant- give K and Cl
Hypophosphatemia
Etiology
Reduced oral intake with GI diseases
Excess use of diuretics, antacids, alcoholism
Alkalosis, treatment of DKA
Effects
Platelets don’t aggregate well
Impaired WBC chemotaxis, phagocytosis
Decreased 2,3 DPG-lower O2 release to tissues
Increased weakness and tremors
Bone pain, malaise, anorexia
Hypophosphatemia
Diagnosis
Suspect during recovery from ketoacidosis or
severe malnutrition
Usually several days after start of Rx for
primary problem
Treatment
Prevent problem with adequate nutrition
If PO4 given watch Ca levels-may fall
Hyperphosphatemia
 Etiology
Renal failure, acidosis
Increased PO4 and Vit D intake
Hypoparathyroidism
 Effects
primarily those of renal failure, acidosis, hypocalcemia
 Treatment
Treat underlying cause
Increase renal PO4 excretion with saline and Diamox
Decrease gut absorption with oral PO4 binders
Exam Answers...
“H2O is hot water and CO2 is cold water.”
Test Question
Serum potassium
A. rises with progressive alkalosis
B. rises with hemolysis
C. is exchanged with glucose at the cell
membrane
D. is independent of serum magnesium
and phosphate
Test Question
Serum potassium
A. rises with progressive alkalosis
B. rises with hemolysis
C. is exchanged with glucose at the cell
membrane
D. is independent of serum magnesium
and phosphate
Test Question
SIADH is characterized by all of the
following except
A. hyponatremia
B. elevated urine sodium concentration
C. contracted extracellular volume
D. high urine specific gravity
E. low urine output
Test Question
SIADH is characterized by all of the
following except
A. hyponatremia
B. elevated urine sodium concentration
C. contracted extracellular volume
D. high urine specific gravity
E. low urine output
SIADH
Laboratory findings in diagnosis of SIADH include:
•Euvolemic hyponatremia <134 mEq/L, and POsm <275
mOsm/kg OR ( POsm - Serum [Urea]mmol/l < 280 mOsm/kg )
•Urine osmolality >100mOsm/kg of water during hypotonicity
•Urine sodium concentration >40 mEq/L with normal dietary
salt intake
Other findings:
•Clinical euvolemia without edema or ascites
•Low blood urea nitrogen (BUN)
•Normal serum creatinine
•Low uric acid
•Normal Acid-Base, K+ balance
•Normal Adrenal, Thyroid function
Test Question
A 60 yo W with primary hyper PTH suffers a femur
fracture. Two days later she undergoes ORIF. On
second postop day, she is extremely drowsy and
vomited several times. Her serum Ca is 15 and her BUN
is 70. She is transferred to the SICU. The most
appropriate treatment at this time would be
A. lasix and calcitonin
B. saline infusion followed by lasix
C. mithramycin and lasix
D. phosphate infusion and lasix
E. lasix followed by emergency parathyroidectomy
Test Question
A 60 yo W with primary hyper PTH suffers a femur
fracture. Two days later she undergoes ORIF. On
second postop day, she is extremely drowsy and
vomited several times. Her serum Ca is 15 and her BUN
is 70. She is transferred to the SICU. The most
appropriate treatment at this time would be
A. lasix and calcitonin
B. saline infusion followed by lasix
C. mithramycin and lasix
D. phosphate infusion and lasix
E. lasix followed by emergency parathyroidectomy
Acidosis
Lines of defense
Lung: anion accumulates in ECF
Increase of 10 torr PACO2 = 0.8 decrease in pH
Plasma buffers: NaHCO3/H2CO3
Nahemoglobinate, Na2HPO4, Na proteinate
Kidney: protects against both acidosis and
alkalosis, great flexibility
Acid-Base Disorders
Respiratory acidosis- increased PCO2,
decreased pH
Respiratory depression-MSO4, CNS injury
Pulmonary disease
Treat with intubation, ventilation, correction
of pulmonary defect
Acid-Base Disorders
Respiratory Alkalosis- decreased PCO2,
increased pH
Hyperventilation due to pain, hypoxia, CNS
injury, ventilator
decreased HCO3 with compensation
danger related to K+ depletion
Treatment directed to underlying cause
Severe, persistent alkalosis may be difficult
to treat
Acid-Base Disorder
Metabolic Acidosis- decreased pH,
decreased HCO3
Normal anion gap - diarrhea, RTA, sm. Bowel
fistula, ureterosigmoidostomy
Elevated anion gap - shock, diabetes,
starvation, ETOH, uremia, methanol, AsA
Treatment directed to underlying cause
Bicarb is generally not a good idea
Metabolic Acidosis
Symptoms:
Kussmaul respiration
Decreased CO
Disorientation
Lethargy, weakness
Decreased myocardial contractility (pH <
7.2)
Dehydration
Metabolic Acidosis
Treatment
Correct shock
Treat diabetes
Increase renal perfusion, etc
Na Lactate- rarely used
Na Bicarbonate- tends to make lactic acidosis
worse
Tris/THAM buffer-works with CHF, liver failure
Dichloroacetate: lowers lactate levels
Acid-Base Disorder
Metabolic Alkalosis - increased pH, increased
HCO3
Causes: Vomiting or excessive gastric suction,
diuretics, increased adrenal corticoids, aldosterone,
excessive bicarb, lg vol citrated blood, Bartter’s
syndrome (hyperaldo)
Treatment consists of replacing fluid losses with
isotonic saline and K, acetazolamide (reabsorb Cl),
arginine hydrochloride
May need to use 0.1N HCl for 6-24 hr period