Ch 17: Fluid and Electrolytes; Acid Base Imbalances Flashcards
Increased with poor kidney function. Imbalances cause cardiac problems. Major intracellular cation. Excrete 90% through kidneys. Normal levels 3.5-5.0
Potassium
Determines whether water is retained, excreted, or moved. Imbalances cause neuro problems. Major cation in the ECF. Normal levels 135-145.
Sodium
Works with sodium to maintain osmotic pressure. Increased with poor kidney function. Decreased with excessive vomiting or diarrhea. Major ECF anion. Normal 96-106.
Chloride
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).
Calcium
Balance is intertwined with calcium Major anion within the cell. Increase in calcium–> decrease of this anion. Normal 3.0-4.5
Phosphate
Normal 6-20. Renal function. Waste in blood from protein digestion. Ammonia to liver–> ____ ____ nitrogen.
0.6-1.3
BUN
Creatinine clearance
If there is an increase in creatinine and no change in BUN, you should look for problems in the ____
liver
How to remember electrolyte levels
“the magic fours.” K+: 4; Cl-: 104; Na+: 140; pH: 7.4; CO2: 40; HCO3: 24
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.
Osmolarity and osmolality
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).
Urine specific gravity
Normal fluid spacing
First spacing
Edema
Second spacing
Ascites, burn edema. Massive amount of fluid that we can’t bring back into normal areas of the body.
Third spacing
Fluids with the same osmolality as the cell interior. No net movement of water occurs. NS, D5W, LR
Isotonic
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.
Hypotonic
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
Hypertonic.
If a person is heme____, give fluids to dilute to bring fluid into the cell. Use ____tonic or ____tonic solutions.
hemeconcentrated; isotonic; hypotonic
If a person is heme___, the concentration is increased with _____tonic solutions.
hemediluted; Hypertonic
Gerontologic considerations
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)
Fluid and electrolyte imbalances
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)
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
Fluid volume excess
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
Fluid volume deficit
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
Sodium
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
Hypernatremia
Hypernatremia treatment
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])
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
Hyponatremia
Treatment of hyponatremia
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
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.
Potassium
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.
Hyperkalemia
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
Hyperkalemia
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.
Hyperkalemia
What you can do for hyperkalemia
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.
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)
Hypokalemia
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.
Hypokalemia
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.
Hypokalemia
What you can do for hypokalemia
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+).
Potassium administration
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.
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.
Calcium
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)
Hypercalcemia
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.
Hypercalcemia
Treatment for hypercalcemia
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
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)
Hypocalcemia
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.
Hypocalcemia
Treatment of hypocalcemia
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
Normal: 3.0-4.5 mg/dL
Phosphate
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
Hyperphosphatemia
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
Hypophosphatemia
Normal is 1.3-2.1 mg/dL
Magnesium
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.
Hypermagnesemia
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
Hypomagnesemia
Lasix. Causes a loss of K+
Loop diuretics
Potentiates digoxin. causes a loss of K+
Thiazide diuretics
Spironolactone, triamterene. Decreased clearance of digoxin and lithium, too much K+ can be harmful
K+ sparing diuretics
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
Electrolytes
Binds with K+ to remove it from the body. Liquid or powder can be given as an enema. Antacids can decrease the effectiveness.
Kayexalate.
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
Acidosis
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)
Respiratory acidosis
Treatment of respiratory acidosis
Patent airway. Oxygen (won’t correct it). TCDB. Semi-Fowler’s position. Suction. Incentive spirometer. Decreased use of sedatives. Bronchodilators. May need ventilator.
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]).
Metabolic acidosis
Treatment for metabolic acidosis
Identify and treat the cause. Insulin for DKA. IV fluids for dehydration. IV bicarbonate. antiemetics for vomiting. Antidiarrheals for diarrhea.
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).
Alkalosis
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)
Respiratory alkalosis
Treatment of respiratory alkalosis
Breathe into paper bag. Oxygen by rebreather mask. Anti-anxiety medication. Relaxation techniques. Reduce stimulation. Treat pain/fever.
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]).
Metabolic alkalosis
Treatment of metabolic alkalosis
Most difficult to treat, slow to resolve. Antiemetics. Fluids. Diamox can stimulate bicarb excretion through the kidneys. No antacids or IV bicard.
How to answer acid-base questions
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]).
