Fluid, Electrolyte, and Acid-Base Balance Flashcards
Body fluids are distributed in two distinct compartments. Briefly explain each one.
a. Extracellular: outside the cells (1/3 of total body water)
b. Intracellular: inside the cells (2/3 of total body water)
Cations:
ions that are positively charged; sodium, potassium, calcium, and magnesium
Anions:
ions that are negatively charged; chloride, and bicarbonate
mmol/L:
represent the number of milligrams of the electrolyte divided by its molecular weight that are contained in a liter of the fluid being measured; (how labs report electrolyte measurements)
osmosis -
process by which water moves through a membrane that separates fluids with different particle concentrations
osmotic pressure -
an inward-pulling force caused by particles in the fluid
osmolarity -
a measure of the number of particles per kilogram of water
isotonic solution -
fluid with the same concentration of nonpermeant particles as normal blood
hypertonic solution -
is more concentrated than normal blood
hypertonic solution -
is more dilute than the blood
diffusion -
passive movement of electrolytes or other particles down the concentration gradient (from areas of higher concentration to areas of lower concentration)
filtration -
fluid moves into and out of capillaries (between the vascular and interstitial compartments)
List the three processes that maintain fluid homeostasis.
A fluid intake and absorption
B fluid distribution
C fluid output
Define how antidiuretic hormone (ADH) regulates fluid balance.
ADH regulates the osmolarlity of the body of fluids by influencing how much water is excreted in the urine. More ADH is released if body fluids become more concentrated. Factors that increase ADH levels: severely decreased blood volume (dehydration, hemorrgage), pain, stressors, and some medications. ADH levels decrease if body fluids become too dilute. This allows more water to be excreted in urine, creating a larger volume of dilute urine and concentrating the body fluids back to normal osmolality. (example, alcohol decreases ADH release, and when people drink they urinate frequently.)
Changes in renal perfusion initiate the renin-angiotension-aldosterone mechanism. Explain the mechanism.
RAAS regulates extracellar fluid volume by influencing how much sodium and water are excreted in urine.
Angiotension I:
Renin converts angiotensionogen to angiotensin I, which other enzymes in the lung capillaries convert to angiotensin II.
Angiotension II:
has several functions, vasoconstriction in some vascular beds. The important fluid homeostatsis function of angiotensin II includes stimulation of aldosterone release form the adrenal cortex
aldosterone
circulates to the kidneys where it causes resorption of sodium and water in isotonic proportion in the distal renal tubules. Removing sodium and water from the renal tubules and retuning it to the blood increases the volume of the extracellular fluid. Contributes to electrolyte and acid base balance by increasing urinary excretion of potassium and hydrogen ions
What is atrial natriuretic peptide?
Regulates ECV by influencing how much sodium and water are excreted in the urine; so opposes the effect of aldoesterone
Potassium
3.5 – 5.0 mEq/L; Maintains resting membrane potential of skeletal, smooth, and cardiac muscle, allowing for normal muscle function
Calcium
9.0 – 10.5; Influences excitability of nerve and muscle cells; necessary for muscle contraction
Magnesium
1.5 – 2.5; Influences function of neuromuscular junctions and is a cofactor for numerous enzymes
Phosphate
2.5 – 4.5 Necessary for production of ATP, the energy source for cellular metabolism
Extracellular fluid volume deficit:
insufficient isotonic fluid in the extracellular compartment
Extracellular fluid volume excess:
too much isotonic fluid in the extracellular compartment
Hypokalemia labs
Serum K+ levels less than 3.5 mEq/L , possible ECG abnormalities
Hypokalemia s&s
Bilateral muscle weakness that begins in quadriceps and may ascend to respiratory muscles, abdominal distention, decreased bowel sounds, constipation, cardiac dysrhythmias, signs of digoxin toxicity at normal digoxin levels
Hyperkalemia labs
Serum K+ level greater than 5 mEq/L possible ECG abnormalities
Hyperkalemia s&s
Bilateral muscle weakness that begins in quadriceps, transient abdomical craps and diarrhea, cardiac dysrhythmias, cardiac arrest
Hypocalcemia labs
Total serum Ca 2+ less than 8.4 mg/dL or serum ionized Ca2+ levels less than 4.5 mg/dL; ECG abnormalities possible
Hypocalcemia s&s
Positive chvostek’s sign, positive trousseau’s sign and circumoral region, hyperactive reflexes, muscle twitching and cramping, tetany, seizures, larygospams, cardiac dyrhythmias
Hypercalcemia labs
Total serum Ca 2+ less than 10.5 mg/dL or serum ionized Ca2+ greater than 5.3 mg/dL; ECG abnormalities possible
Hypercalcemia s&s
Anorexia, N&V, constipation, fatigue, diminished reflexes, lethargy, decreased level of consciousness, confusion, personality change, cardiac dysrhythmias; possible flank pain from renal calcuil; shift of calcium from bone, pathological fractures; signs of digoxin toxicity at normal digoxin levels
Hypomagnesemia labs
Serum Mg2+ level less than 1.5 mEq/L
Hypomagnesemia s&s
Positive Chvostek’s and Trousseau’s signs, hyperactive deep tendon reflexes, insomia, muscle cramps and twitching, grimacing, dysphagia, tachycardia, hypertension, tetany, seizures, cardiac dysrhythmias; signs of digoxin toxicity at normal digoxin levels
Hypermagnesemia labs
Serum Mg2+ level greater 2.5 mEq/L; ECG abnormalities possible
Hypermagnesemia s&s
Lethargy, hypoactive deep tendon reflexes, bradycardia, hypotension, acute elevation in magnesium levels; flushing, sensation of warmth; severe hypermagnesemia; flaccid muscle paralysis, decreased reate and depth of respirations and cardiac dysrhythmias, cardiac arrest
