306 Fluids and Electrolytes

• Intracellular: body cells
• Extracellular: 
• -tissue space between cells
• -blood that fills the vascular compartment
• -transcellular (3rd space-- CSF, peritoneal, joints)

• Cerebral Spinal Fluid
• Pepritoneal Cavity
• Joints

• Transports gases, nutrients and wastes
• Generates electrical activity
• Transforms food into energy
• Maintains overall function

• **Environmental Stress and Disease
• –Increase fluid loss

–Impair fluid intake

• –Interfere with mechanisms that regulate fluid volume,
• composition, and distribution

ICF & ECF

Intracellular Compartment (ICF)

Extracellular Compartment (ECF)

60%

40% body weight

20% body weight

• *Large amounts of sodium (Na+) and chloride (Cl-)
• *Moderate amounts of bicarbonate (HC03-)
• *Small quantities of potassium (K+), calcium (Ca+2), magnesium (Mg+2), and Phosphate (P+)

•Large amounts of potassium (K+)

• •Small amounts of sodium,
• chloride, bicarbonate, and phosphate

•Moderate amounts of magnesium

•Almost no calcium

Electrolytes

• DO NOT
• (ex: Glucose does NOT dissociate)

Diffusion

Osmosis

Solutes

• ex: 
• Blood= +water, -solute
• Cell= -water, +solute
• (water rushes in cell toward the solute)

Osmolarity

280 - 295 mOsm/L

Tonicity

How much they cause a cell to shrink or swell

neither shrink nor swell (equal)

Cell swells

Cell shrinks

Particles

Fluid

• •Factors favoring movement out of capillary
• –Capillary filtration pressure
• (hydrostatic pressure)
• –Interstitial colloid pressure
• (tissue oncotic pressure)

• •Factors favoring the movement of fluid back into the capillary
• –Capillary colloid osmotic pressure (plasma proteins)
• –Tissue Hydrostatic pressure

Lymph drainage 

–Increase in the capillary filtration pressure (Ex: dependent edema)

• –Decrease in the capillary colloidal osmotic pressure (loss of
• serum proteins); burns, kidney and liver disease

–Increased capillary permeability

–Obstruction to lymph flow - lymphedema

•Daily weight

•Visual assessment

•Measurement of the affected part

•Application of finger pressure to assess for pitting edema

•Accumulation in transcellular spaces (Ex: CSF, peritoneal, joints)

•Contributes to body weight but not to fluid reserve or function

•Peritoneal cavity - acites

•Pleural cavity - hydrothorax

• Liquids/Foods
• Metabolic reactions

–Respiratory tract (expiration)

–GI tract

–Skin (perspiration)

–Kidneys (urine our put)

135-147 mEq/L

• –Controls ECF osmolality
• –Participates in active transport (Na+/K+ pump)
• –Action potentials of muscle, neuron

GI, Meds, IV solutions

•kidney, GI, skin

–Vomiting, diarrhea, enemas, sweat, burns can increase sodium losses

Kidney

• It retains sodium when arterial pressure is low.
• It eliminates sodium when arterial pressure is high.

• Sympathetic Nervous System and the renin-angiotensin-aldosterone system (RAAS).
• Aldosterone increases reabsorption of Na
• Atrial Natriuretic Peptide (ANP) decreases reabsorbtion.

Thirst

Adipsia

Hypodypsia

Polydipsia

Antidiuretic Hormone (ADH)

–Thirst --->  increased water intake

–ADH release ---> water reabsorbed from urine

–Lack of thirst ---> decreased water intake

–Decreased ADH release ---> water lost in urine

• •Severe pain
• •Nausea
• •Trauma
• •Surgery
• •Certain anesthetic
• •Some analgesic drugs 

Deficiency or decreased response to blood volume

•Central or neurogenic diabetes insipidus 

Nephrogenic diabetes insipidus 

Excessive urination, excessive thirst (if not able to communicate thirst – dehydration)

•Failure of normal negative feedback system to inhibit ADH – most often from neoplasias, lung and neurologic diseases

•Retention of H2O even when serum sodium levels are too low (dilutional hyponatremia).

•Increase GFR suppresses RAA system

•Suppression of aldosterone → low sodium reabsorption. Serum Na osmolality low; Urine osmolality high

• Hypotonic hyponatremia
• Natriuresis
• Urine osmolality exceeds plasma osmolality
• Other blood values may also be low

•Inadequate fluid intake

•Excessive gastrointestinal fluid losses

•Excessive renal losses

•Excessive skin losses

•Third-space losses

•Inadequate sodium and water elimination

•Excessive sodium intake in relation to output

•Excessive fluid intake in relation to output, water intoxication

Isotonic Fluid Volume Deficit 

• –Inadequate fluid intake, excessive GI, renal, or skin losses
• –Third space losses

–Weight loss;

–Increased: ADH, thirst, urine osmolality and SG;

–Decreased: urine output, loss of skin or tissue turgor, BV and BP

Isotonic Fluid Replacement

Isotonic Fluid Volume Excess

• –Decrease in Na and H2O elimination by kidney
• (CHF, RF)
• –Excessive Na intake, meds, IV fluids
• Cushing’s syndrome – corticoid increases Na retention

–Wt gain, edema, increased blood volume and pressure, pulmonary edema

diuretics, restricted Na diet

Hyponatremia

Excessive sodium losses, inadequate sodium intake, replacement with Na free fluids; excessive water intake, SIADH

Hypotonic (dilutional) hyponatremia

hypervolemic

Hypovolemic

Isovolemic

Hypertonic hyponatremia

GI (abdominal cramps, N/V/), headache, changes in LOC, seizures, (coma -cerebral edema), edema, muscle cramps, weakness, fatigue, 

•–Lab values, signs & symptoms; loop diuretics, saline solutions

Hypernatremia

Infants and Children

–Excessive intake of Na (salt water drowning, IV )

–Loss of water (diarrhea, excessive sweating, hypertonic tube feedings, diabetes insipidus)

–Inability to respond to thirst

Dehydration: Wt loss, thirst, dry mucous membranes, decreased urine output and BV (tachycardia, weak thready pulse), loss of tissue turgor, agitation, coma

Lab values; Replacement of fluids (ORT)

•Normal level is 3.5-5.5 mEq/L

•Maintains intracellular osmolarity

•Controls cell resting potential

•Needed for Na+/K+ pump

•Exchanged for H+ to buffer changes in blood pH

Decreases; Increases

• Gains – dietary
• Losses – mainly by kidney

• Regulations: 
• –Kidney – Regulates retention and elimination of K+.

•Aldosterone causes K+ to be

•K+-H+ shift: When K+ is increased in serum: K+ secreted into tubule, H+ reabsorbed into blood → drop pH, metabolic acidosis. If serum K+ ↓: K+ reabsorbed, H+ secreted → rise in pH, metabolic alkalosis

–Transcellular shifts between intracellular and extracellular as needed to regulate K levels

 

Transcellular Shift to regulate K

Hypokalemia

Poor nutrition, excessive losses (GI, renal, skin), diuretics

CV- EKG changes, dysrhythmias

Postural hypotension

GI- anorexia, N/V, constipation, paralytic ileus

Neuromuscular- weakness, fatigue

Muscle cramps

Paresthesia

CNS- irritability, confusion

Acid-base disorders

Lab values; Dietary, oral supplements, IV

• Lowers
• (cells fire less easily)

Hyperkalemia

–Excessive intake of potassium (oral potassium supplements, infusion of potassium containing parenteral fluids

–Release from intracellular compartment (Burns, tissue trauma, crushing injury, extreme exercise)

• Inadequate elimination by kidneys
• -Renal failure, adrenal insufficiency, (Addison’s decr aldosterone)

Neuromuscular- initially- muscle cramps

Then, inactivation of sodium channels- decrease excitability and Paresthesia Cardiovascular- Serious- EKG changes

Lab values, symptoms, ECG; Calcium can reverse membrane excitability, IV glucose & insulin cause K+ to → cells. Dietary restrictions

• RAISES
• –Cells fire more easily
• –When resting potential reaches threshold, Na+ gates open and won’t close

• Calcium
• Phosphate
• Magnesium

–Ingested in the diet

–Absorbed from the intestine

–Filtered in the glomerulus of the kidney

–Reabsorbed in the renal tubules

–Eliminated in the urine

Normal serum level 8.5 – 11.0 mg/dL

• *Most is stored in bone
• *Blocks sodium gates
• *Clotting
• *Intracellularly needed for muscle contraction
• *Acts as a messenger in hormone and neurotransmitter pathways

• *Vitamin D- Maintains plasma levels of calcium and phosphate by increasing
• *Intestinal absorption

PTH- low calcium levels cause a release of PTH, removing calcium from bone, decreasing calcium elimination from kidney,  increasing phosphate elimination

• *Hypoparathyroidism (low PTH)- yields hypocalcemia
• *Hyperparathyroidism (high PTH)- yields hypercalcemia
•  
• *Calcitonin- decreases  serum calcium levels, stores excess in bone

*Calcium balance inverse to phosphate- If calcium decreases, phosphate increases

 

Serum calcium < 8.5 mg/dL

–Impaired ability to move Ca from bone: Decreased PTH (hypoparathyroidism, Mg deficiency, Vit D deficiency)

–Abnormal losses (from kidney, pancreatitis)

Protein binding– alkalosis causes Ca to bind to protein, lowering free levels

–Blocks Na channels, so nerves fire more easily: Paresthesia, tetany, muscle cramps, convulsions

–Chvostek’s and Trousseau’s sign

–CV – hypotension, cardiac arrhythmias (heart block, V fib), failure to respond to calcium mediated drugs (digitalis, NE, dopamine)

Lab values: ↓Ca, ↓PTH, ↑Phosphate; Acute: IV calcium solutions; Chronic: oral and dairy supplements

Trousseau's Sign -- ischema-induced carpal spasm that can occur with hyopcalcemia or hypomagnesia

Serum calcium > 11.0 mg/dL

–Increased intestinal absorption (Excessive Vitamin D and calcium, milk-alkali syndrome – calcium + antacids)

• –Increased bone resorption - Increased levels of parathyroid
• hormone, malignant neoplasms, prolonged immobilization

–Decreased elimination - Thiazide diuretic, lithium therapy

–Blocks more Na channels, decreased neural excitability, muscle weakness, lethargy, stupor, coma

–CV – increased contractility, hypertension, AV block

–GI – anorexia, N/V, constipation, pancreatitis

–Renal – kidney stones, impair concentration of urine, thirst, polyuria

•Lab values, symptoms; Rehydration, diuretics to eliminate Na and Ca in urine

•Plays a major role in bone formation

•Essential to certain metabolic processes:

–The formation of ATP and the enzymes needed for metabolism of glucose, fat, and protein

•Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane

•Serves as an acid-base buffer in the extracellular fluid and in the renal excretion of hydrogen ions

•Needed for normal function of red blood cells, white blood cells and platelets

•PTH promotes bone loss of P into serum

2.0-6.0 mg/dL

Serum phosphate < 2.0 mg/dL

 

–Malnutrition, insufficient intestinal absorption - high Mg, Ca, Al inhibit absorption of P (antacids), glucocorticoids, alcoholism

–Transcompartmental shifts - insulin moves glucose and P into cells.

–Increased renal losses –DKA, drugs

• **Same as increase in calcium
• Blood- platelet and WBC impairment, hemolytic anemia
• Neuro- tremors, confusion, coma
• Musculoskeletal- bone pain, osteomalacia, Rickets

Dietary, oral, or IV replacement therapy

Serum phosphate > 6.0 mg/dL

–Failure of kidneys to excrete P (RF)

–Shift of P from ICF to ECF (burns, tissue injury)

–Ingestion of phosphates (laxatives, antacids, enemas)

**Same as decrease in calcium (see hypocalcemia)

•Lab values; Dietary restriction, phosphate binders, hemodialysis ESRD

•Cofactor in rx (essential for ATP)

•Involved in DNA replication, transcription

•Assists Na/K pump

•Heart contraction

•Necessary for PTH function

•Nerve conduction, ion transport, binds to Ca receptors

•Regulation: Ingested in diet, excreted by kidneys. Reabsorption stimulated by PTH, inhibited by ↑Ca levels

•Mg and K levels change together: ↓Mg = ↓K

1.8-2.4 mg/dL

Serum magnesium < 1.8 mg/dL

–Malnutrition, excessive Ca intake, alcoholism, diuretics, DKA

–Neuromuscular – ↑ in excitability, muscle weakness, tetany, + Babinski’s, Chvostek’s, Trousseau’s signs, disorientation, psychotic symptoms

–Cardiovascular - Tachycardia, hypertension, cardiac dysrhythmias

–Often occurs in combination with hypocalcemia and hypokalemia

Serum magnesium > 2.4 mg/dL

–Excessive intake: laxatives, Mg antacids, IV administration of magnesium for treatment of preeclampsia, excessive use of oral magnesium-containing medications

Decreased Excretion: Kidney disease, Acute renal failure

–↑Mg suppresses PTH → hypocalcemia, blocks ACh release → muscle weakness, blockade, or respiratory paralysis

–CV – Hypotension, ↓ BP, arrhythmias

Neuro – Confusion, coma, hyporeflexive

Lab values; IV calcium