Study Fluids Electrolytes

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

“3 rd 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)


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 SoluteHypotonic = 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 WATER

We use “osmolality” when we talk about osmotic pressure in the human body.

Expressed as Osmols or milliOsmols per LITER of SOLUTION

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


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

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.


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.


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.

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.


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.


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.

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.


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.

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.

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.


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!


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.


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.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.

Study Fluids Electrolytes

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