Ch 17: Fluid and Electrolytes; Acid Base Imbalances

Question 1

Increased with poor kidney function. Imbalances cause cardiac problems. Major intracellular cation. Excrete 90% through kidneys. Normal levels 3.5-5.0

Answer 1

Potassium

Question 2

Determines whether water is retained, excreted, or moved. Imbalances cause neuro problems. Major cation in the ECF. Normal levels 135-145.

Answer 2

Sodium

Question 3

Works with sodium to maintain osmotic pressure. Increased with poor kidney function. Decreased with excessive vomiting or diarrhea. Major ECF anion. Normal 96-106.

Answer 3

Chloride

Question 4

Transmission of nerve impulses, heart and muscle contractions, blood clotting, formation of teeth and bone. Requires vitamin D for absorption. Bound to albumin=inactive (normal 8.6-10.2). Free from albumin=ionized=active (normal 4.4-5.4).

Answer 4

Calcium

Question 5

Balance is intertwined with calcium Major anion within the cell. Increase in calcium–> decrease of this anion. Normal 3.0-4.5

Answer 5

Phosphate

Question 6

Normal 6-20. Renal function. Waste in blood from protein digestion. Ammonia to liver–> ____ ____ nitrogen.
0.6-1.3

Answer 6

BUN

Creatinine clearance

Question 7

If there is an increase in creatinine and no change in BUN, you should look for problems in the ____

Answer 7

liver

Question 8

How to remember electrolyte levels

Answer 8

“the magic fours.” K+: 4; Cl-: 104; Na+: 140; pH: 7.4; CO2: 40; HCO3: 24

Question 9

Indicates the water balance of the body. Serum is 285-295 mOsm/kg. High is water deficit (concentrated). Low is water excess (dilute).
Urine is 50-1200 mOsm/kg (avg: 500-800). Low-not concentrating urine appropriately. High= urine too concentrated.Together are used to determine what is causing a sodium imbalance.
Amount of solutes in the blood. Can also tell through serum sodium levels.

Answer 9

Osmolarity and osmolality

Question 10

Measures the kidney’s ability to concentrate or dilute urine.
1.003-1.030:
High is concentrated. Low is dilute or unable to concentrate. Kidney failure often causes a fixed specific gravity (1.010).

Answer 10

Urine specific gravity

Question 11

Normal fluid spacing

Answer 11

First spacing

Question 12

Edema

Answer 12

Second spacing

Question 13

Ascites, burn edema. Massive amount of fluid that we can’t bring back into normal areas of the body.

Answer 13

Third spacing

Question 14

Fluids with the same osmolality as the cell interior. No net movement of water occurs. NS, D5W, LR

Answer 14

Isotonic

Question 15

Solutions in which the solutes are less concentrated than in the cells. Hypoosmolar. If a cell is surrounded by this type of fluid, water moves into the cell, causing it to swell and possibly burst. 1/2 NS.

Answer 15

Hypotonic

Question 16

Fluids with solutes more concentrated than in cells, or an increased osmolality. Hyperosmolar. If this type of fluid surrounds a cell, water leaves the cell to dilute the ECG; the cell shrinks and may eventually die. 3% saline, D10W

Answer 16

Hypertonic.

Question 17

If a person is heme____, give fluids to dilute to bring fluid into the cell. Use ____tonic or ____tonic solutions.

Answer 17

hemeconcentrated; isotonic; hypotonic

Question 18

If a person is heme___, the concentration is increased with _____tonic solutions.

Answer 18

hemediluted; Hypertonic

Question 19

Gerontologic considerations

Answer 19

Percent of body weight of water is decreased. Structural changes in the kidney and decreased renal blood flow (decreased GFR, decreased creatinine clearance, loss of ability to concentrate urine and thus conserving water [can’t selectively reabsorb], decrease in renin and aldosterone, increased in ADH and ANP).
Loss of subcutaneous tissue. Decrease in thirst mechanism. Musculoskeletal changes. Mental status changes. Incontinence (don’t drink water=more dehydration)

Question 20

Fluid and electrolyte imbalances

Answer 20

Can occur in healthy people.
Can be life threatening: elderly; chronic renal and endocrine pts; pts taking medications that affect fluid and electrolyte balance (diuretics, TPN, tube feedings)

Question 21

Causes: too much intake (hypertonic fluids), renal failure (no excreting=stays in body=backs up=overload=hemedilution), heart failure, liver failure.
Body compensates by suppressing ADH to increase urine output to decrease BP and volume.
S/S: weight gain, edema, ascites, high BP, bounding pulses, crackles, JVD
Labs: low sodium and osmo (sometimes), low specific gravity, low HCT

Answer 21

Fluid volume excess

Question 22

Causes: too little intake, NPO, diabetes (mellitus or insipidous), burns, wound drainage, sweating, diarrhea, vomiting, diuretics, hemorrhage, 3rd spacing.
Body compensates by increasing thirst, releasing ADH (reabsorb water), increasing aldosterone to decrease urine output and raise BP and volume
S/S: weight loss, dry mucosa, low BP, tenting, elevated temp
Labs: high sodium and osmo (sometimes), high specific gravity, high albumin, high Hct, high BUN

Answer 22

Fluid volume deficit

Question 23

Major cation of ECF. Reflects the ratio of ___ to water. Regulated by kidneys, ADH, aldosterone. GI tract absorbs it from food, expels it through urine and sweat. Imbalances are typically associated with fluid volume problems. Foods high in ___- processed meats, condiments, dairy
Normal levels: 135-150 mEq/L

Answer 23

Sodium

Question 24

Water loss or sodium gain.
Hypovolemic: decreased total body weight and sodium with a relatively greater decrease in TBW (d/t GI losses, burns, osmotic diuresis [high glucose], loop diuretics, infection).
Hypervolemic: increase sodium with normal or increased TBW (d/t endocrine problems [primary aldosteronism], too much salt intake [oral or IV], renal failure)
Euvolemic: decreased TBW with near normal total body sodium (d/t DI, increased insensible loss).
Hyperosmolality: shift of water out of the cells leading to cellular dehydration (shrinking) and subsequent brain injury
Neurologic (from cell shrinkage) or relate to what is causing the water loss
s/s: altered mental status, lethargy, seizures, increased HR, decreased BP; other s/s from the cause of the water loss

Answer 24

Hypernatremia

Question 25

Hypernatremia treatment

Answer 25

Treat the underlying cause
Diuretics (after you have looked at the other s/s: promotes sodium loss or stop them (depending on the cause)
Sodium restriction
Seizure precaution.
Decreased water is cause: water replacement, isotonic/hypotonic fluids.
Increased Na+ is cause: salt-free IV solutions, diuretics, decreased Na+ intake (avoid high sodium foods). isotonic/hypotonic IV fluids.
Dialysis.
If d/t DI, may need to give ADH (vasopressin [AVP, DDAVP])

Question 26

Water excess or loss of sodium.
Hypervolemic: dilution form. occurs when there is an increase in total body water but a relatively smaller increase in total serum sodium. CHF, cirrhosis, renal failure.
Hypovolemic: losing H20 and Na+. GI loses, 3rd spacing, diuretics, Addison’s disease
Euvolemic: dilutional for. occurs when the total serum sodium is normal or near normal, but the total body water is increased without clinically evident edema. SIADH, diuretics, hypothyroid, psychogenic polydipsia

Answer 26

Hyponatremia

Question 27

Treatment of hyponatremia

Answer 27

3% NS (increases osmolality because it is hypertonic): IV hypertonic saline. Increase sodium content in the vascular fluid. Water for fluid overload (crackles, edema, bounding pulses).
If c/b fluid excess: fluid restriction, osmotic diuretics (i.e. mannitol. causes excretion of water but not sodium).
SIADH treat with lithium or declomycin

Question 28

Major cation of the ICF. Normal 3.5-5.0 mEq/L. Sodium-potassium pump is a major controller. Moves into cells during formation of new tissues and leaves the cell during tissue breakdown. Source- diet. Primary route of loss- kidney. Foods: avocado, fish, banana, OJ, raisins, dried fruits, meat, milk, fruits, veggies, salt substitutes.

Answer 28

Potassium

Question 29

Causes: kidney failure (most common), salt or potassium supplements, cell destruction, acidosis (H+ for K+ exchange with cells), hypoxia, catabolic state, K+-sparing diuretics, hemolyzed blood, adrenal insufficiency.
Can get false high results if the specimen is not handled properly.

Answer 29

Hyperkalemia

Question 30

Increased cell excitability, takes less stimuli to excite, cellular action potential may discharge spontaneously.
Muscle weakness, cramping leg pain progressing to areflexia, diarrhea (increased peristalsis), abdominal cramping, nausea, oliguria

Answer 30

Hyperkalemia

Question 31

When you think of sx associated with cardiac problems, think “heart”- it disrupts electrical conduction.
Cardiac depolarization is decreased- flattening P wave, widening of the QRS.
Repolarization is increased: shortening of QT interval, T wave narrower and more peaked.

Answer 31

Hyperkalemia

Question 32

What you can do for hyperkalemia

Answer 32

Cardiac monitor. Kayexelate. Calcium gluconate (reverse cardiac membrane excitability). Glucose and IV insulin (drives K+ into cells). Sodium bicarb (acidosis). Loop/thiazide diuretics (if kidneys are functioning). Stop K+ in IV fluids. Have pt avoid foods high in K+. Dialysis if severe.

Question 33

Causes: vomiting, NG suction, diarrhea, medications (diuretics, laxatives, insulin), metabolic alkalosis (not enough acid in blood. Cell gives H+ but takes K+). Rapid cell building (i.e. B12 or erythropoietin to increase RBCs). Insulin therapy. Low sodium and magnesium levels (low serum Mg++ at renal tubules will automatically trigger aldosterone=reabsorb H20 and Na+ and excrete K+). Stress (catecholamine release)

Answer 33

Hypokalemia

Question 34

Decreased excitability of cells, especially in nerves and muscles, making them less responsive to stimuli.
Dysrhythmias, weakness, N/V, paralytic ileum, constipation, low BP, weak pulse, muscle weakness and paralysis.
Increased digoxin toxicity. Diuresis.
Beta blockers decrease HR and preload. Can become hyper because decrease shift of K+ into the cell.

Answer 34

Hypokalemia

Question 35

Impaired repolarization.
Peaked P wave. QRS prolonged. Flattening T wave. Emergence of U wave as a result of messing with the T wave. Increased depolarization.

Answer 35

Hypokalemia

Question 36

What you can do for hypokalemia

Answer 36

Cardiac monitor. Foods high in K+ (fruit juice, citrus fruits, dried fruits, bananas, nuts, veggies). Watch for dig toxicity. K+ IV (only if good urine output). Magnesium (if magnesium is low, we will never bring K+ up). Hold HCTZ, Lasix, cortisone (synthetic steroid=reabsorption of Na+ and H20=excrete K+).

Question 37

Potassium administration

Answer 37

MUST have urine output (>30 mL/hr).
NEVER give IV push or undiluted.
MUST be on cardiac monitor.
Assess IV site often (prefer CVC)
Give no more than 40 mEq in a 50-100 mL bolus
Run no faster than 20 mEq/hr
Give no more than 40 mEq/L in IV maintenance fluids.

Question 38

Normal is 8.5-10.2. Stored in our bones, but to absorb it, we must have vitamin D. Get it from dietary intake and absorption in the intestines. Regulated by parathyroid hormone, calcitonin, and vitamin D.
Affects transmission of nerve impulses, heart and muscle contractions, blood clotting, an forming of teeth and bone.
Free (ionized; what does the reactions ) vs bound (attached to proteins/albumin): ionized should be 4.4-5.4 mg/dL.
Has in inverse relationship with phosphorus.

Answer 38

Calcium

Question 39

Causes: hyperparathyroidism. Malignancy (esp breast cancer, lung cancer, multiple myeloma). Vitamin D or calcium overdose. Prolonged immobilization. Renal failure. Use of thiazide diuretics.
Ionized Ca++: acidosis (causes albumin to release Ca++ or decreases its binding to albumin)

Answer 39

Hypercalcemia

Question 40

Reduces excitability of muscles and nerves.
Lethargy, confusion, depressed reflexes, severe muscle weakness, fractures, kidney stones, constipation, faster clotting times (risk of DVT).
SLOWS EVERYTHING DOWN.

Answer 40

Hypercalcemia

Question 41

Treatment for hypercalcemia

Answer 41

Promotion of excretions of calcium in urine with a loop diuretic (i.e. Lasix)
Isotonic IV fluids
Hydration with isotonic saline (promotes excretion of calcium- drink 3000-4000 mL daily).
Synthetic calcitonin IM/SQ (inhibits calcium resorption from bone)
Weight bearing activity
Bisphosphonates (Pamidronate, Zoledronic Acid): hypercalcemia c/b malignancies. inhibit osteoclasts breakdown of bone.
No antacids (most have calcium).
Dialysis/Cardiac monitoring

Question 42

Causes: Removal of parathyroid gland (can’t regulate Ca++ levels). Acute pancreatitis (inhibition of absorption). Multiple blood transfusions (citrate can strip the body of Ca++). Alkalosis (increased binding of ionized Ca++. Total Ca++ may be fine but ionized will be low). Immobility. Lactose intolerance. Malabsorption syndromes, decreased vitamin D intake. Renal failure. Drugs (i.e. citrate, mitramycin, Calcibind). Increased phosphorus. Post-menopausal women.
Causes of decreased ionized calcium: alkalosis (increases binding to albumin)

Answer 42

Hypocalcemia

Question 43

S/S: tetany. Trousseau’s sign. Chvostek’s sign. STRIDOR. Numbness/tingling around the mouth/extremities. Cardiac sx (change in HR, thready pulse). Leg or foot cramps. Abd cramps/diarrhea; if chronic may have brittle bones.

Answer 43

Hypocalcemia

Question 44

Treatment of hypocalcemia

Answer 44

Oral/IV calcium supplements (never given IM).
Diet high in calcium (i.e. broccoli, dairy, spinach)
Vitamin D supplemts
Very closely observe those who have had thyroid or neck surgery

Question 45

Normal: 3.0-4.5 mg/dL

Answer 45

Phosphate

Question 46

Causes: renal failure, tumor lysis syndrome.
Most symptoms are usually d/t the low calcium instead of the phosphorus.
S/S: calcium deposits in joints, skin, kidneys, eyes; hypocalcemia, tetany, neuromuscular irritability
Tx: fix hypocalcemia

Answer 46

Hyperphosphatemia

Question 47

Causes: malnutrition, malabsorption syndrome, alcohol abuse, too many antacids.
S/S: CNS depression (increase in calcium slows things down), confusion, muscle weakness, dysrhythmias, fractures.
Tx: oral supplements (Neutra-Phos), decrease calcium intake, IV phosphate (but this can cause sudden hypocalcemia), stop antacids and calcium supplements
Decreased cellular excitability because missing a key component of ATP

Answer 47

Hypophosphatemia

Question 48

Normal is 1.3-2.1 mg/dL

Answer 48

Magnesium

Question 49

Cause: increased intake (i.e. MOM, Maalox), chronic kidney disease
S/S: lethargy, N/V, loss of DTRs, can have respiratory and cardiac arrest.
Tx: avoid magnesium-containing drugs, increased fluid intake, may need dialysis.
DECREASES CELLULAR EXCITABILITY.

Answer 49

Hypermagnesemia

Question 50

Cause: prolonged fasting or starvation, chronic alcoholism, diuretics.
S/S: confusion, hyperactive DTRs, tremors, seizures, cardiac dysrhythmias
Tx: oral supplements, increase green veggies, nuts, bananas, oranges, peanut butter, chocolate; IV or IM magnesium (if given too rapidly can cause cardiac or respiratory arrest)
INCREASES CELLULAR EXCITABILITY

Answer 50

Hypomagnesemia

Question 51

Lasix. Causes a loss of K+

Answer 51

Loop diuretics

Question 52

Potentiates digoxin. causes a loss of K+

Answer 52

Thiazide diuretics

Question 53

Spironolactone, triamterene. Decreased clearance of digoxin and lithium, too much K+ can be harmful

Answer 53

K+ sparing diuretics

Question 54

Potassium is most common. Have to have good urine output, should not exceed 40 mEq/L in IV fluids. Should never exceed a rate of 10-20 mEq/hr

Answer 54

Electrolytes

Question 55

Binds with K+ to remove it from the body. Liquid or powder can be given as an enema. Antacids can decrease the effectiveness.

Answer 55

Kayexalate.

Question 56

Labs: low pH, low bicarb, high CO2, high K+
Makes many drugs ineffective.
Decreases force of cardiac contraction.
Decreases vascular response to catecholamines.
Causes increased release of the oxygen molecule from hemoglobin

Answer 56

Acidosis

Question 57

Cause: Retention of CO2. Respiratory depression (narcotics, sedatives, anesthesia). Inadequate chest expansion (chest wall deformity, abd distention, spinal cord injury, neuromuscular disease). Airway obstruction (pneumonia, PE, etc). CNS depression (head injury)

Answer 57

Respiratory acidosis

Question 58

Treatment of respiratory acidosis

Answer 58

Patent airway. Oxygen (won’t correct it). TCDB. Semi-Fowler’s position. Suction. Incentive spirometer. Decreased use of sedatives. Bronchodilators. May need ventilator.

Question 59

Causes: Acid excess (DKA, seizures, starvation). Acid retention (resp or renal failure). Bicarb deficit (dehydration, diarrhea, pancreatitis).
Anion gap in the presence=loss of bicarb (Sodium - [Chloride + Bicarb]).

Answer 59

Metabolic acidosis

Question 60

Treatment for metabolic acidosis

Answer 60

Identify and treat the cause. Insulin for DKA. IV fluids for dehydration. IV bicarbonate. antiemetics for vomiting. Antidiarrheals for diarrhea.

Question 61

Labs: low Ca++ (ionized=tetany, stridor), low K+ (taking K+ from blood in exchange for H+), high pH, high bicard, low CO2
Interferes with tissue oxygenation and normal neuromuscular function.
Affinity for O2 to Hgb increases. Still will have normal SpO2 because Hgb is holding onto O2 fine, but it is not releasing it to tissues (measurement of SvO2 would be high, >80).

Answer 61

Alkalosis

Question 62

Causes: Loss of acids. Hyperventilation (pain, fever, anxiety, sepsis, pregnancy, thyrotoxicosis, improper vent settings). CNS stimulation (fever, tumors, drugs-ASA, catecholamines). Hypoxemia (asphyxiation, high altitudes, shock. PE, asthma, pneumonia)

Answer 62

Respiratory alkalosis

Question 63

Treatment of respiratory alkalosis

Answer 63

Breathe into paper bag. Oxygen by rebreather mask. Anti-anxiety medication. Relaxation techniques. Reduce stimulation. Treat pain/fever.

Question 64

Causes: Increased bicarb (too many oral antacids, citrates from multiple blood transfusions, TPN, lactate in dialysis [lactate is converted to bicarb in liver], IV bicarb). Increased loss of acids (prolonged vomiting, NG suction, too much diuretics [lose H+ as well]).

Answer 64

Metabolic alkalosis

Question 65

Treatment of metabolic alkalosis

Answer 65

Most difficult to treat, slow to resolve. Antiemetics. Fluids. Diamox can stimulate bicarb excretion through the kidneys. No antacids or IV bicard.

Question 66

How to answer acid-base questions

Answer 66

Identify the metabolic problem first (DKA or high glucose=metabolic acidosis; vomiting or NG suction=metabolic alkalosis; diuretics=metabolic alkalosis).
Identify respiratory alkalosis next: hyperventilation (i.e. pain, fever, anxiety, high resp rate, hypoxia sx or causes)
Whatever is left is respiratory acidosis (too sedated, immobility, lung problems affecting oxygen exchange [ie pneumonia, PE, chest damage]).