Study Session: Fluids; Electrolytes; Acid/Base Balance

September 6, 2006

PART I: FLUID BALANCE (Presented by Jamie Moran)

Fluid Spaces

“Intracellular”: Inside the Cells

“Extracellular”: Outside the Cells

“Intravascular”: Inside the vessels

“Interstitial”: Between the cells and vessels

“3rd Space”: Same space as interstitial, but usually refers to fluid that is not available for use
by the body.

Fluid Movement

“Diffusion” (Latin: To spread out) The process in which particles in a fluid move from an area of higher
concentration to an area of lower concentration resulting in an even distribution of the
particles in the fluid. Little to no energy is required. (Mosby’s Dictionary)

“Osmosis” Movement of a pure solvent (water) through a differentially-permeable membrane from a

solution that has a lower solute concentration to one that has a higher solute concentration.
The membrane is impermeable to the solute but is permeable to the solvent (water). The
rate of osmosis depends on the concentration of solute, the temperature of the solution, the
electrical charge of the solute and the difference between the osmotic pressures exerted by
the solutions. Movement across the membrane continues until the concentrations of the
solutions equalize. Little to no energy is required. (Mosby’s Dictionary)

“Filtration” Process whereby fluid and solutes move together across a membrane from one
compartment to another. The movement is from an area of higher concentration/pressure to
lower concentration/pressure. Also called “Facilitated Diffusion”. Requires little to no
energy. (Kozier & Erb)

“Active Transport” Movement of materials across the membranes and epithelial layers of a cell by
means of chemical activity that allows the cell to admit otherwise impermeable molecules
against a concentration gradient. Requires carrier molecules and energy from ATP.
(Sodium/Potassium pump is an example of active transport.) (Mosby’s Dictionary)
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Pressure

Fluid-PUSHING Pressure
“Hydrostatic Pressure”

“Capillary Pressure”

“Intravascular Pressure”

“Blood Pressure”

Fluid-PULLING Pressure

The pressure exerted on a differentially permeable membrane separating a solution from a solvent
(Mosby’s Dictionary). The pressure depends on the CONCENTRATION of a solution.

Hypertonic =Higher Concentration of Solute

Hypotonic = Lower Concentration of Solute
Isotonic = Same Concentration of Solute
“Osmotic Pressure” – general term for the force of osmosis (any solute)

“Crystalloid Pressure” – term for the force of osmosis related to a salt or electrolyte (commonly
Sodium)

“Oncotic Pressure” – term for the force of osmosis related to a protein (commonly Albumin)

“Plasma Colloid Pressure” – same as “Oncotic Pressure” except specific to proteins in the blood
vessels.

Osmolality/Osmolarity

Definition: Measurement of the osmotic pressure of a solution

OSMOLALITY OSMOLARITY
Expressed as Osmols or milliOsmols per KG of Expressed as Osmols or milliOsmols per LITER
WATER of SOLUTION
We use “osmolality” when we talk about
osmotic pressure in the human body.

In the human body, the solutes included in the measurement of osmotic pressure are:
Sodium, Glucose and Urea.

(2 x serum Na) + (BUN/3) + (Glucose/18) = Serum Osmolality

Normal Range: 280 to 295 mOsm/KG of water. (Aigner and Potter & Perry)

For IV solutions, the isotonic range is 240 to 340 mOsm

Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Regulation of Fluid Movement

Organs/Glands/Hormones

Hypothalamus Thirst mechanism

Pituitary Gland ADH (anti-diuretic hormone) – released in response to a decrease in blood
volume or an increase in sodium concentration; it triggers the reabsorption of water
in the renal tubules.
Kidneys Urine production; Renin/Angiotensin – released in response to decreased renal
perfusion, it increases blood pressure by stimulating the release of Angiotensin II and
Aldosterone.
Lungs Angiotensin II – increases blood pressure by constricting blood vessels and
deactivating bradykinin, a vasodilator.
Adrenal Cortex Aldosterone – a steroid hormone that acts in the renal tubules to retain
sodium and/or excrete potassium (to increase blood volume).
Heart ANP (ANF) (Atrial Natriuretic Peptide/Factor) – a hormone released by the atria of
the heart in response to increased blood volume and vasoconstriction. It causes
natriuresis, diuresis and renal vasodilation and reduces concentrations of
Renin/Angiotensin, ADH and Aldosterone (to reduce blood volume).

Fluid Imbalances

Fluid Volume Deficit

Dehydration: Low water volume = increased osmolality
Result: Cells shrink
Caused by: Any situation that increases fluid loss
Signs/Symptoms: Changes in mental status, dizziness, weakness, extreme thirst.
Fever, dry skin, poor skin turgor; increased heart rate, lower blood
pressure; low and/or concentrated urine output; in severe cases seizures
and coma.
Testing: Elevated hematocrit; elevated serum osmolality; elevated serum sodium
level; elevated urine specific gravity
Treatment: Replace fluids. Use only hypotonic, low-sodium IV fluids (D5W) infused
slowly over 48 hours. Too rapid infusion will create edema.

Hypovolemia: Isotonic loss of fluid (water plus solutes/electrolytes)

Result: Low blood volume; decreased perfusion
Caused by: Excessive bleeding; excessive sweating; diabetes mellitus; diuretics; fever;
NG drainage; vomiting/diarrhea; excessive urination; 3rd space shifting
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Signs/Symptoms: Mild cases: thirst; increased heart rate; orthostatic hypotension;

restlessness; anxiety; delayed capillary refill; cool/pale skin of extremities;
weight loss; confusion; irritability. Serious cases: SHOCK
Testing: Difficult to test for hypovolemia: Normal osmolality; Look for decreased
hemoglobin and HCT; elevated BUN; increased urine specific gravity.
Treatment: IV fluid challenges: large volume, rapid infusions of normal saline and/or
LR followed by infusion of plasma proteins/albumin. In cases of
hemorrhage, blood transfusion may be required. Vasopressor and
Dopamine help support blood pressure and oxygen therapy helps with
tissue perfusion.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Fluid Volume Excess

Hypervolemia: Isotonic gain of fluid (water plus solutes/electrolytes); causes high blood volume
Result: Edema; pulmonary edema; congestive heart failure
Caused by: Excessive sodium or fluid intake; fluid or sodium retention; renal failure;
hypertonic IV fluids; infusion of plasma proteins.
Signs/Symptoms: Elevated blood pressure; weight gain; pitting edema; crackles in
lungs (pulmonary edema); shortness of breath; increased, then decreased
cardiac output; rapid, bounding pulse; distended veins; tachypnea.
Testing: Low HCT (hemodilution); normal sodium; low potassium and BUN (or
higher levels, if renal failure); low oxygen levels; pulmonary congestion on
xrays.
Treatment: Restrict sodium and fluid intake; diuretics; vasodilators
(nitroglycerin/morphine); heart failure treated with digoxin; hemodialysis;
oxygen treatment and bedrest.

Water Intoxication: High water volume = decreased osmolality

Result: CellsSwell
Caused by: Excessive low-sodium fluid intake; SIADH (head trauma; tumors;
medications); rapid infusion of hypotonic IV solutions (D5W); tap water
enemas and tap water NG tube irrigation
SIADH: 80% caused by oat cell carcinoma of the lungs; CNS dysfunction
(stroke/brain trauma); Medications (antidepressants; chemo; narcotics;
neuroleptics; carbamazepine; psychotropics)
Signs/Symptoms: Increased intracranial pressure (headache; personality change;
behavior change; confusion); nausea; vomiting; cramping; muscle
weakness; thirst; twitching; dyspnea on exertion and dulled senses.
Testing: Low serum sodium levels; decreased serum osmolality.
Treatment: Treat underlying cause; restrict fluid intake and avoid use of hypotonic IV
solutions; hypertonic IV fluid should only be used in severe cases to draw
fluid out of the cells, and should be accompanied by close monitoring of
the patient.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

PART II: ELECTROLYTES (Presented by Shanna Dyals)

CATIONS

SODIUM
Important to note-
There are two types of hypo/hypernatremia, thus four sets of symptoms and treatments to understand.
The symptoms and treatments vary depending upon what the cause of the imbalance is. Keep this in mind
when discussing this electrolyte.
Function: Fluid balance, transmission of nerve impulses, muscle contractions, acid/base
imbalance, MAJOR determinate of fluid volume.
Location: Mainly in extracellular space
Normal range:135-145 mEq/L
R/T Electrolytes: Inverse relationship with Potassium, affinity for Chloride
Sources: Canned foods, processed foods

Hypernatremia
Scenario 1: Caused by: Inadequate water intake/excessive water loss. Water loss
r/t high fever, heatstroke, diabetes insipidus, osmotic diuresis
(diabetes).

Symptoms: Many of the symptoms are r/t dehydration. The symptoms marked with
an asterisk are r/t hypernatremia. Intense thirst*, dry swollen tongue,
restlessness*, agitation*, twitching*, seizures*, coma*, weakness,
postural hypotension, decrease CVP, weight loss.
Treatment: Same as for dehydration: Replace fluids. Use only hypotonic, low-
sodium IV fluids (like D5W) infused slowly over 48 hours. Too rapid
infusion will create edema (especially in the brain).

OR

Scenario 2: Caused by: Sodium Gain. Sodium gain r/t IV hypertonic solutions, IV
sodium bicarbonate, IV excessive isotonic NaCl, primary
hyperaldosteronism, saltwater near drowning.

Results in: Mainly nuerologic symptoms, dehydration, shrinking cells (especially in

the brain) and increased excitability of neurons.

Symptoms Many of these symptoms are r/t increased fluid volume. The symptoms
marked with an asterisk are r/t hypernatremia. Intense thirst*,
restlessness*, agitation*, twitching*, seizures*, coma*, flushed skin,
weight gain, peripheral and pulmonary edema, increased BP, and
increased CVP.

Treatment Dilute the excess Sodium with D5W and promote excretion of excess
Sodium and water with diuretics.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

So, for both cases of hypernatremia the symptoms are intense thirst, restlessness, agitation,
twitching, seizures, and coma. The variable symptoms are dependent on whether hypernatremia is
r/t fluid loss or sodium gain.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Hyponatremia

Scenario 1: Caused by: Excess water intake/ decreased water elimination. Water
gain r/t SIADH, Congestive heart failure, excessive hypotonic IV fluids,
primary polydipsia.

Results in: Cellular swelling especially in the brain.

Symptoms Many of the symptoms are r/t fluid volume excess. The symptoms
marked with an * are r/t hyponatremia. Headache, lassitude, apathy,
weakness, confusion*, nausea*, vomiting*, weight gain, increased BP,
increased CVP, muscle spasm, seizures*, coma*.

Treatment: Fluid restriction. If severe symptoms develop, intravenous hypertonic

3% NaCl.
OR

Scenario 2: Caused by: Sodium loss. Sodium loss r/t GI losses (diarrhea,
vomiting, fistulas, NG suction), renal losses (diuretics, adrenal
insuffiency, Na+ wasting renal disease) and skin losses (burns, wound
drainage).

Results in: Cellular swelling especially in the brain.

Symptoms: Many of these symptoms are r/t fluid volume deficit, the symptoms
marked with an * are r/t hyponatremia. Irritability, apprehension,
confusion*, postural hypotension, tachycardia, rapid, thready pulse,
decreased CVP, decreased jugular venous filling, nausea/vomiting*, dry
mucous membranes, weight loss, tremors, seizures*, coma*.

Treatment: Fluid replacement with sodium containing solutions or oral rehydration

fluids containing electrolytes.

So, for both cases of hyponatremia, the symptoms are confusion, nausea/vomiting, seizures, and
coma. The other symptoms are dependent on whether the hyponatremia is r/t fluid excess of
sodium loss.

Remember: The key symptoms for hypo/hyernatremia remain constant. The water balance that is
involved just ADDS other symptoms to the list. If you know the symptoms of water volume excess and
water volume deficit you can figure the rest of the symptoms out.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

POTASSIUM

Function: Transmission and conduction of nerve impulses, cardiac rythyms, and smooth
muscle contraction, and cell building. Potassium is VERY important for cardiac
function, any alteration will have serious cardiac effects.
Location: Mainly in intracellular space
Normal range:3.5 – 5.0 mEq/L
R/T Electrolytes: Inverse relationship with Sodium; decreased amounts of Magnesium can
cause decreased amounts of Potassium
Sources: Fruits, dried fruits, and vegetables

Factoids: * Factors that cause Potassium to move from ECF to ICF are insulin, B-adrenergic
stimulation, and rapid cell building.

* Factors that cause Potassium to move from ICF to ECF are acidosis, trauma to cells,
and exercise.
* Potassium is the drug of choice for lethal injection. Lethal amounts cause the heart
to stop pumping upon administration.

Hyperkalemia
Caused by: Increased Potassium intake (IV administration, potassium containing drugs, or
salt substitutes), impaired renal excretion (RENAL FAILURE), shift of Potassium
from ICF to ECF (acidosis), burn or crush injury, tumor lysis, rapid transfusion
of aged blood. Some drugs such as Potassium sparing diuretics and ACE
inhibitors decrease renal excretion of Potassium.
Results in: Membrane potential changes
Symptoms: Irritability, anxiety, abdominal cramping, diarrhea, , weakness of lower
extremeties, leg pain, parathesias, irregular pulse, ventricular fibrillation, and
cardiac standstill (think lethal injection). Changes in EKG.
Treatment: Decrease Potassium intake, increase Potassium elimination (kayexelate and
increased fluids), force Potassium out of ECF into ICF using insulin, IV sodium
bicarbonate (to correct underlying acidosis). Dangerous cardiac arrythmias
require administration of Calcium Gluconate IV. Hemodialysis for patient with
renal failure.

Hypokalemia
Caused by: Abnormal shift of Potassium for ECF to ICF (alkalosis and anemia), abnormal
losses of Potassium via GI tract (diarrhea, laxative abuse, ileostomy drainage)
or kidneys. Hyperaldosteronism, Magnesium deficiency. Associated with Tx of
diabetic ketoacidosis (increase urinary losses and admin. Of insulin. Also can
be caused by starvation, a diet low in Potassium, or IV fluids with no
Potassium if NPO.
Results in: Membrane potential changes;
Symptoms: Weak, irregular pulse, ventricular arrhythmias, bradycardia, digoxin toxicity,
skeletal muscle weakness, paralysis (esp. in legs), muscle cramping and cell
breakdown (rhabdomyolysis), nausea/vomiting, polyuria, hyperglycemia,
decreased smooth muscle function (paralytic ileus, altered airway
responsiveness). EKG changes.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Treatment: Potassium chloride supplement and increase in dietary Potassium. Potassium

is NEVER given IV push, 10- 20 mEq/hr is recommended. Watch for rebound
hyperkalemia and cardiac arrest.

Remember: Potassium can have disastrous lethal effects on the heart. Many of the symptoms
of hypokalemia can be confused for diabetes (polyuria, hyperglycemia). I like to remember the
GI effects of Potassium by saying hypo-- less potassium--causes less GI activity, paralytic ileus.
And that hyper- more potassium--causes more GI activity, diarrhea. Both types of Potassium
imbalances affect the lower legs and cause irregular pulse.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

CALCIUM

Functions: Formation of bones and teeth, nerve impulse transmission, myocardial contraction,
blood clotting, ,muscle contractions, and blocking of Sodium at the cellular level.

Regulation: Parathyroid hormone is secreted by the parathyroid gland. It increases the amount of
Calcium absorbed and available for use.

Calcitonin (hormone)is secreted by the Thyroid gland. It decreases the amount of

Calcium absorbed and available for use.

Location: Mostly in bones (serves as a reserve of Calcium) Three types are found in serum: (1)
bound to protein-mostly albumin; (2) Free or ionized (represented in the 4.5 –5.5
mEq/L measurement). This is the chemically active Calcium; and (3) Complexed with
phosphate, citrate, or carbonate. Almost half of the serum calcium is ionized.

Normal Range: Serum- 9 - 11 mg/dl Ionized- 4.5 - 5.5 mEq/L

R/T electrolytes: Inverse relationship to Phospate, and decreases in Calcium occur commonly
with decreases in Magnesium.

Sources: Milk, leafy green vegetables, tums, calcium supplements.

Hypocalcemia
Caused by: Decreased total calcium-Chronic renal failure, elevated phosphorus (inverse
rel.), Primary hypoparathyroidism or injury to the parathyroid gland, Vitamin D
deficiency, Magnesium deficiency (connected rel.), acute pancreatitis, Loop
diuretics, alcoholism, diarrhea, or decreased serum albumin. Decresed ionized
calcium-alkalosis (increased PH increases calcium binding, which decreases
ionized Calcium), excess administration of citrated blood.
Result in: Increasing nerve excitability
Symptoms: Tiredness,depression, anxiety confusion, numbness and tingling circumoral,
hyperreflexia, laryngeal spasm, tetany, seizures, and decreased cardiac
contractility.
Chvostek’s sign (Tapping a facial nerve causes facial contraction)
Trousseau’s sign (Carpal spasm induced by inflating a BP cuff)
Treatment: Treat the cause. Oral or IV calcium supplements. Vitamins high in Calcium and
Vitamin D.

Hypercalcemia
Caused by: Increased total calcium caused by multiple myeloma, other malignancy,
prolonged immobilization, hyperparathyroidism, hypothyroidism,Vitamin D
overdose, and Thiazide diurectics. Occurs rarely from increased Calcium
intake r/t diet and antiacids.
Increased ionized Calcium caused by acidosis (decrease in PH decreased
calcium binding, thus increasing ionized Calcium).
Results in: Decreased nerve excitability
Symptoms: Lethargy, weakness, depressed reflexes, confusion, personality changes,
psychosis, anorexia, N/V, bone pain, fractures, polyuria, dehydration, stupor,
coma, and ventricular arrythmias, constipation, renal calculi.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Treatment: Promote excretion of Calcium with diuretics, encourage patient to drink 3-4
liters/day to decrease calculi formation. Possible administration of synthetic
Calcitonin, and encourage weight bearing activity.

Remember: The symptoms in Calcium imbalances are directly r/t the effect on
membrane polarization. Less Calcium=more excitability and more activity. Ex. Tetany,
seizures, anxiety, hyperreflexia, muscle cramps, ect. More calcium=less excitability. It
slows everything down. Ex. Lethargy, confusion, decreased memory/reflexes, stupor,
coma.

ANIONS

PHOSPHORUS/PHOSPHATE

Functions: Essential to function of muscles, RBC enzyme, ATP and nervous system.

Location: Primary anion in the intracellular fluid (I like to think of it as P with P, potassium and
phosphate)

Normal range: 2.8 - 4.5 mg/dl

R/T Electolytes: Inverse relationship to Calcium

Sources: Milk, dairy products, or phosphate-containing drugs and laxatives

Hyperphosphatemia

Caused by: Renal failure (Phospate is not eliminated), chemo, increase ingestion of milk or
phosphate containing laxatives, Vitamin D overdose.

Results in: Precipitates and high phosphate levels with low Calcium levels.

Symptoms: Calcified deposits in skin, soft tissue, cornea, viscera, and blood vessels. Other
symptoms are r/t concurrent hypocalcemia such as muscle problems and
tetany.

Treatment: Identify and treat cause. Restrict food and fluids high in phosphorus, correct
hypocalcemic conditions. Provide adequate hydration. Phosphate binding gels
such as Renagel, may be necessary.

Hypophospatemia

Caused by: Malabsorption syndrome, TPN, alchohol withdrawal, phosphate binding

antiacids, respriratory alkalosis.

Results in: Deficiency of ATP and fragile RBC

Symptoms: Central nervous systems dysfunction: confusion, coma, rhadomylysis, cardiac

problems (arrhythmia), muscular weakness, osteomalacia.

Treatments: Oral supplementation of phosphorus, dairy products, Iv admin. Of sodium

phosphate or potassium phosphate. Sudden symptomatic hypocalcemia can
occur with admin. Of IV phosphate.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Remember, many of the symptoms of hyperphosphatemia are directly linked to the

inverse relationship between calcium and phosphorus. Many of the symptoms are a
result of the hypocalcemia superimposed of the hyperphosphatemia. Many of the
symptoms associated with hypophosphatemia are a result of the loss of Potassium for
cellular f(x) such as RBC enzymes and ATP production. The central nervous system dysfx
(confusion/coma) and muscle weakness happen because the fragile RBC’s and
decreased ATP cause less Oxygen to be available for the body.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

MAGNESIUM
Functions: Metabolism of cellular nucleic acids, carbohydrates, and proteins. Magnesium acts
directly on the myoneural junction and neuromuscular excitability is affected.

Location: In the intracellular fluid, mainly in bones (50-60%)

Normal range: 1.5 - 2.5 mEq/L

R/t electrolytes: Factors that influence Calcium levels (PTH) appear to influence Magnesium
levels. Many Magnesium imbalances are mistaken for Calcium imbalances.

Sources: Maalox, milk of magnesia, green vegetables, nuts, bananas, oranges, peanut butter,
chocolate. TIP:I like to remember Magnesium goes with Calcium because Magnesium
and Calcium sound similar to each other. The other electrolyte, Phosphate, has an
inverse relationship with Calcium and sounds nothing like it.

Hypermagnesemia
Caused by: Renal failure, magnesium sulfate administration for eclampsia during
pregnancy, other Magnesium containing drugs, and adrenal insuffiency

Results in: Depressed neuromuscular and CNS function-similar to hypocalcemia.

Symptoms: Initially lethargy, drowsiness, N/V. May progress to loss of deep tendon
reflexes, somnolence, respiratory and cardiac arrest.

Treatment: Focus is on prevention. Patients with renal failure should be taught to avoid
magnesium-containing drugs such as Maalox and Milk of Magnesia. Severe
hypermagnesemia may be treated with IV Calcium Chloride or Calcium
Gluconate. Increase fluids as well to increase Magnesium elimination. Patients
with renal failure will require dialysis because the kidneys are the major route
of excretion for Magnesium.

Hypomagnesemia
Caused by: Prolonged fasting or starvation, chronic alcoholism (decreased intake and
increased urinary output), parental nutrition w/out Magnesium, fluid loss from
GI tract and fluid loss r/t uncontrolled diabetes.

Results in: Neuromuscular and CNS hyperirritability

Symptoms: Confusion, hyperactive deep tendon reflexes, tremors, seizures, and cardiac
arrest.

Treatment: Oral Magnesium supplementation, increase dietary Magnesium. In severe

cases, IV Magnesium sulfate.

Remember, Magnesium imbalances are easy. The signs and symptoms are VERY similar
to Calcium imbalances. Even doctors confuse the two!
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

PROTEINS

ALBUMIN / OTHER PLASMA PROTEINS

Functions: Contribute to colloid osmotic pressure determining plasma volume.

Location: Found mostly in the intravascular space, some in the interstitial space.

Normal range:6 - 8 g/dl

R/t electrolytes Decreased albumin can decrease serum Calcium.

Sources: Meat products, beans

Hyperproteinemia

Caused by: Is rare but can result from dehydration- induced hemoconcentration.

Hypoproteinemia

Caused by: Anorexia, malnutrition, strarvation, fad dieting, vegetarian diets. Poor
absorption r/t pancreatic insufficiency and inflammatory bowel disease. Shift
from intravascular space r/t inflammation. Increased breakdown of protein due
to fever, sepsis, and maliganancies. Protein loss r/t massive burns. Increased
use r/t wound healing and cell growth. Hemorrhage with loss of protein.
Impaired protein synthesis in liver.

Results in: Decreased amount of protein resulting in decreased colloid osmotic pressure,
tissue breakdown, fatigue, protein released into interstitial space.

Symptoms: Edema, anorexia, fatigue, slow wound healing, muscle loss, and ascites.

Treatment: High carbohydrate, high protein diet, and dietary protein supplements. May
need enteral nutrition orTPN.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

WHY???

I found the symptoms easier to understand if I knew why they happened. Here are explanations that I hope
will help you remember them too.

Sodium-
Diabetes insipidus leads to hypernatremia b/c it causes large amounts of dilute urine to be lost leaving
behind lots of sodium.
Osmotic Diabetes (regular diabetes) leads to hypernatremia because large amount of urine are lost leaving
behind lots of sodium.
Primary hyperaldosteronism causes hypernatremia b/c excess Sodium is retained r/t increasesed
aldosterone levels.
SIADH (syndrome of inappropriate antidiuretic hormone) causes hyponatremia b/c more water is retained
diluting serum sodium.
Congestive Heart Failure (CHF) causes sodium to be diluted with retained water resulting in hyponatremia.
Primary polydipsia (excess thirst) causes sodium to be diluted with excess water resulting in hyponatremia.
Hypoaldosteronism causes sodium to be lost because not enough aldosterone is secreted to maintain
normal serum sodium levels resulting in hyponatremia.

Potassium-
Acidosis causes hyperkalemia b/c hydrogen ions shift into cells in exchange for potassium. It raises the
amount of K+ in the ECF.
Burn/crush/tumor lysis all cause injury to cells releasing K+ from the ICF to the ECF resulting in
hyperkalemia.
Transfusion of aged blood leads to hyperkalemia b/c the aged blood cells have broken down and released
their K+ to the ECF.
Alkalosis causes hypokalemia because hydrogen ions in the cells are exchanged for K+ ions in the ECF. K+
shifts from ECF to ICF causing low serum K+ levels.
Tx of anemia causes K+ to shift into ICF b/c K+ is needed for RBC formation.
Hyperaldosteronism causes increased Na+ levels and decreased K+ levels (remember the inverse
relationship) This results in decreased smooth muscle contraction causing decreased bowel activity and
altered airway responsiveness.

Calcium-
Decreased Ca+ causes nerve excitability because Ca+ blocks Na+ at the cellular membrane in Ca+
channels.
Hypoparathyroidism causes not enough Ca+ to be retained resulting in hypocalcemia.
Acute pancreatitis causes hypocalcemia because it releases a substance that binds with calcium thus
decreasing Ca+ levels.
Loop diuretics and diarrhea cause more Ca+ to be lost through the GI tract resulting in hypocalcemia.
Infusion of citrated blood causes Ca+ to bind with citrate forming a calcium-citrate complex. This
decreases the ionized Ca+level.
Hypothyroidism-less calcitonin causes less Ca+ to be excreted.
Malignancy causes Ca+ to be released r/t bone destruction and parathyroid related hormones secreted by
the tumor. This results in hypercalcemia.
Prolonged immobilization causes hypercalcemia r/t bone breakdown by osteoclasts.
Hyperparathyroidism causes more Ca+ to be retained resulting in hypercalcemia.
Renal calculi result from increased Ca+ in renal tubules in hypercalcemia.
Weight bearing activity helps treat hypercalcemia by encouraging Ca+ to be deposited in the bones.

Phospate-
Calcified deposits are a result of increased phosphate binding with Ca+. This leads to hypocalcemia in
conjunction with hyperphophatemia.
Malabsorption syndrome and TPN can cause hypophosphatemia r/t decrease phosphorus intake.

Magnesium-
Renal failure leads to hypermagnesemia because less Mg+ is excreted by the kidneys.
Study Session: Fluids; Electrolytes; Acid/Base Balance
September 6, 2006

Calcium chloride and Calcium Gluconate directly oppose the cardiac effects of hypermagnesemia.

Protein Imbalances-
Decreased protein intake results from anorexia, malnutrition, starvation, and fad diets.
Massive burns cause protein to shift into the interstitial space. The protein pulls water into the interstitial
space resulting in edema.
Slow wound healing results from decreased protein because protein is essential for tissue regeneration.
Muscle is wasted during hypoproteinuria because it is broken down for its protein stores.