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MED SURG TEST #1 fluid and e- tutorial notes

PPT #1 FLUID AND E- (just an intro, terms, simple concepts, etc.)
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___ Space: Liquid found inside the cell
Intracellular
Extracellular Space:
___ (fluid that is in the blood vessels - plasma)
___ (fluid in the space between the cells)
___ (fluid in specialized cavities e.g. cerebrospinal fluid, synovial fluid, pleural fluid.)
Intravascular, Interstitial, Transcellular
pressure created by Plasma proteins. Pulls fluid back into blood vessels at venous end of the capillary bed. Also called oncotic pressure.
colloid osmotic pressure
___ hydrostatic pressure (caused by the pumping action of the heart) pushes water, electrolytes, and nutrients through the capillary walls.

___ colloid osmotic pressure (created by plasma proteins) pulls water, electrolytes, and cell waste products into the capillary through the capillary walls.
Arterial; Venous
The movement of molecules from an area of higher concentration to an area of lower concentration is called:___
diffusion
___: escape of fluid into a part.
effusion
A decrease in serum protein (as in malnutrition, burns, nephrosis, or liver disease) results in low ___ pressure.
colloid osmotic (oncotic)
___ pulls fluid back into blood vessels at the venous end of the capillary bed.
Colloid oncotic pressure
Increased venous hydrostatic pressure, as in heart failure or cirrhosis, prevents water from moving from the interstitial space into the vascular space. The hydrostatic pressure is higher at the venous end of the capillary than the colloid oncotic pressure, so water is not pulled back into the vascular bed. What would be the likely result?
tissue edema
Inflammation, burns, or allergic reaction cause vasodilation and increased capillary permeability, causing both water and solutes to move ___ into the tissues creating tissue edema.
out
___ exert colloid osmotic power (pressure).
___ exert crystalloid osmotic power (pressure).
___ (non-protein, non-electrolyte) exerts osmotic power for water.
Proteins; Electrolytes; Glucose
If H+ (hydrogen) is greater than K+ (potassium) the kidney tubules will secrete H+ instead of K+. The serum K+ will rise. The opposite is true if the H+ level drops. This is an important concept to remember in ___ disorders.
acid-base
Increased potassium levels stimulate aldosterone release form the adrenal gland, which promotes ___ loss in the urine.
K+
If the K+ balance changes, it changes:

___ and
ability of cells to fire
cell excitability. This means that:
Cells will fire excessively with little stimulation
-or-
cells will barely respond to stimulation.
Hypokalemia (low serum potassium) occurs from:
excessive fluid loss from diarrhea, vomiting, nasogastric suction
diuretic drugs (especially loop diuretics like Lasix)
inadequate intake of potassium-rich foods (along with abnormal losses)
draining wounds / fistulas
loss of K+ in urine when the kidney does not reabsorb it
diuresis in uncontrolled diabetes mellitus
excess aldosterone secretion (hyperaldosteronism)
malabsorption syndromes, malnutrion
acid-base imabalances
heart failure (as Na+ and water retained, K+ it lost)
laxative abuse
K+ free intravenous fluids while N.P.O.
trauma, with loss of K+ in urine
intravenous insulin and glucose
stress reaction (excess adrenocortical hormone secretion)
Findings of hypokalemia:
serum K+ < 3.5 mEq/L
generalized muscle weakness, malaise
paresthesias
cardiac dysrhythmias (arrest can occur)
enhanced effects of digitalis (digitalis toxicity)
decreased or absent reflexes (begins in lower extremities)
abdominal pain, vomiting, nausea, anorexia
reduced intestinal peristalsis, intestinal distention with gas, paralytic ileus
decreased blood pressure
metabolic alkalosis
polyuria
Cardiac changes which may occur in hypokalemia include:
forceful contraction
weak pulse
electrocardiogram changes include:
flat or inverted t-waves
U wave present
depressed ST segment
tall P-waves, prolonged P-R interval
wide QRS complex
multifocal PVCs (premature ventricular contractions)
ventricular fibrillation and cardiac arrest
supraventricular and ventricular ectopic beats
increased risk of digitalis toxicity (low K+ makes the heart muscles more sensitive to the action of this drug)
Treatment of hypokalemia includes:
correcting the cause
oral or intravenous administration of potassium (do not use K+ if the urine output is <600 ml/day)
salt substitutes containing K+
foods high in K+, some of these include:
bananas, pears, fresh dried apricots
fruit juices
tea, cola beverages
milk
meat, fish
baked potato
dried beans (cooked)
anything that tastes good—chocolate—mmm...
Excess potassium (hyperkalemia) can be caused by:
decreased excretion of K+ by the kidneys (as in renal failure—obliguria and anuria)
excessive administration of K+
cell trauma which releases intracellular K+
burns, crush injuries, myocardial infarction
extensive surgery, infection
hemolysis of red blood cells
acidosis (e.g. diabetic ketoacidosis)
adrenal insufficiency (Addison's disease)
K+ sparing diuretics which antagonize aldosterone
salt substitutes containing K+
intestinal obstruction
insulin deficit
hemorrhagic shock
Hyperkalemia may be manifested by:
serum K+ > 5.5 mEq/L
bradycardia
fatal dysrhythmias, cardiac arrest
hypotension
generalized muscle weakness, malaise
increasing, ascending, flaccid paralysis leading to respiratory difficulties
irritability, apathy
nausea, diarrhea
electrocardiogram changes
abdominal cramps
hyperreflexia, numbness, tingling
metabolic acidosis
oliguria, anuria
Cardiac changes which may occur in hyperkalemia include:
sluggish, flaccid myocardial muscle action
bradycardia
slowed SA and AV node conduction with excessively high K+
tall, peaked T-waves followed by depressed ST segment
prolonged P-R interval
P-wave flat or absent
QRS widens
prolonged QT interval which leads to arrest
ventrical fibrillation
Treatment of hyperkalemia may include:
calcium to counteract effect of K+ on heart muscle
sodium bicarbonate to alkalinize body fluids (causes K+ to shift from ECF to ICF)
hemodialysis or peritoneal dialysis
cation exchange resins (Kayexalate) by mouth or enema (pulls K+ and water into intestines)
small dose of regular insulin and 50% glucose (intravenously) to aid transfer of glucose and K+ into the cells
restrict dietary K+
You have a patient who received severe thermal burns yesterday. What will happen to the serum K?
serum levels will rise. Yes,
p. Since K+ is dominant inside the cell, if the cell is damaged, K+ will be released into the blood.
You have a patient in metabolic acidosis (high serum hydrogen and low pH). What would you expect to find in lab test results which indicate the body is trying to compensate for this problem?
high serum potassium; increased urinary H+. K+ and H+ exchange with each other in the kidney tubule to try to correct imbalances.
Which one of the following patients on your unit should be observed closely for indications of excessive loss of potassium?
The patient who has:
the flu with frequent, large amounts of emesis and diarrhea
A patient has been taking osmotic diuretics for some time. You would want to obtain an order for serum:
K+
Your patient with severe burns is now one day post-injury. Without treatment, what problem is the patient apt to develop?
hypokalemia. Initially after a thermal burn, K+ will be high since the K+ moves out of the injured cells. However, after a few days, the K+ drops as the excess is eliminated by the kidneys and some begins to move back into cells.
Why does hyperkalemia occur in the patient in metabolic acidosis (excess H+, low pH)?
The kidneys are secreting excess H+ and retaining K+. . In acidosis, the kidney will retain K+ and excrete H+ to try to correct acidosis. Also, K+ moves out of the cell and H+ moves in to be buffered by cell buffers.
The drug ___, pulls potassium and water into the GI tract where it is lost in feces; serum potassium level will drop.
Kayexalate
Na+ affects the fluid volume of the ECF and is regulated, in part, by:
aldosterone
renal blood flow
renin secretion
antidiuretic hormone (ADH) due to its effect on water
estrogens
carbonic anhydrase enzyme
Sodium has important physiologic functions including:
neuromuscular irritability
conduction of nerve impulses and muscle contraction
osmotic pressure of the ECF
acid-base balance
water balance
gland secretions
Sodium imbalances are referred to as osmolar imbalances. There is either too much or too little sodium in relation to the amount of water. The terms are therefore ___ or hypoosmolar.
hyperosmolar
Hyponatremia means a serum sodium level below normal.

It is due to sodium loss (solute deficit) or water gain. This is a hypoosmolar state.

The result of the hypoosmolar imbalance is that water leaves the ECF and moves ___ the cell, causing cell ___.
into; swelling.
Hyponatremia with water excess results from:
excess intake of water/forcing hypotonic fluids
inability of kidneys to excrete water (renal failure)
retention of water (as in heart failure or cirrhosis of the liver)
excess tap water enemas
excess intravenous fluids of dextrose in water
SIADH (syndrome of inappropriate antidiuretic hormone secretion)
True hyponatremia is relatively uncommon. The hypoosmolar state where there is hyponatremia with dehydration (sodium deficit in excess of water) result from:
poor salt intake
diuretic drugs which cause Na+ loss
burn wounds or wound drainage
cystic fibrosis
adrenal insufficiency (Na+ lost in urine)
fluid loss replaced with water only
salt wasting nephritis
excessive gastrointestinal loss
loss of bile
nasogastric suction along with ice chips or water by mouth
using water only for NG tube irrigations
Manifestations of hyponatremia (hypoosmolar state) where there is reduced Na+ and excess water reflect failure of swollen cells to transmit electrical impulses. Neurological symptoms are due to cerebral edema and altered nerve conduction. Findings include:
serum Na+ < 1.35 mEq/L
mental confusion, headache
altered levels of consciousness, coma
hyperirritability, anxiety
tremors, seizures
hyperreflexia, muscles weakness, twitching
nausea, vomiting: abdominal cramps
edema and weight gain
Clinical findings in hyponatremia with dehydration include those of hypovolemia:
serum Na+ < 1.35 mEq/L
hypotension
tachycardia
cold, clammy skin
decreased skin turgor
dry mucous membranes
weight loss
seizures, hyperirritability
In a ___ state, there is too much sodium in relation to the amount of water. There will either be a deficit of body fluid with hypernatremia or hypernatremia in excess of the amount of water.

In either case, the ECF becomes hypertonic, water leaves the cell and the cell shrinks.
hyperosmolar
Causes for hyperosmolar imbalance where there is hypernatremia and fluid deficit include situations when water loss exceeds sodium loss or when there is inadequate water intake. Such situations could include:
decreased water intake due to:
Inability to swallow
mental confusion, loss of consciousness
debilitated state
anorexia, depressed thirst mechanism
inability to communicate need for water
excessive water loss, without sodium loss, through burn wounds, sweating, mechanical ventilation, coughing, polyuria
failure of kidney to reabsorb water
diabetes insipidus
Cushing's syndrome
renal tubular disease
excessive use of osmotic diuretics
Another hyperosmolar imbalance is that where there is excess Na+ in relation to the amount of water. This imbalance represents a gain of sodium without water loss. Water will pour out of cells into the ECF. Causes of this form of hypernatremia include:
excess sodium containing intravenous solutions
excess salt intake
The indication of a hyperosmolar imbalance include:
serum sodium level > 145 mEq/L, serum osmolarity > 295 mOsm/kg
intense thirst
dry, sticky mucous membranes, dry, rough, red tongue
flushed, dry skin, poor skin turgor
oliguria
low-grade fever
weakness, lethargy which can progress to coma
irritability, agitation, convulsions, tremors
increased deep tendon reflexes, nuchal rigidity
circulatory overload, shock, respiratory distress and renal failure can occur if the hyperosmolar state continues
Treatment of hypernatremia, hyperosmolar states, includes:
gradual reduction of serum sodium to prevent cerebral edema
us D5 / ¼ % or .45% saline solution (avoids overcorrection causing deficit)
monitor urine output and serum sodium levels
administer fluids cautiously
restrict sodium intake


Prevention of the problem is the best treatment. Remember, if a person is unable to ask for fluids, or obtain fluids themselves-think of hypernatremia. The person who experiences extreme thirst, who can obtain fluids will not develop hypernatremia.
Calcium is an important electrolyte.
The normal serum calcium level is ___.
About 98% of calcium is stored in the bones and teeth.
About 50% of calcium in the blood is bound to protein.
Muscle cells store calcium.
4.5 - 5.5 mEq/L.
Several factors influence serum calcium levels including:
parathyroid hormone
calcitonin
vitamin D
estrogens and androgens
carbohydrate and lactose
Calcium balance is also influenced by:
absorption of calcium from the gastrointestinal tract
excretion of calcium in urine and feces
deposition and resorption of bone
acid-base balance
Calcium functions in:
muscle contractile ability
correct neural function
development and strength of bones and teeth (also requires vitamin D and phosphorus)
blood clotting
Causes for hypocalcemia include:
insufficient dietary intake of calcium & vitamin D; starvation
hypoparathyroidism, injury to parathyroid glands during thyroidectomy
impaired intestinal absorption from diarrhea, overuse of laxatives or enemas containing phosphorus
chronic malabsorption syndromes
hyperphosphatemia (occurs in renal failure)
alkalosis
hyperproteinemia
chronic renal failure
Cushing's syndrome (excess adrenal hormones)
hypomagnesemia
sepsis
burns
hyperventilation
Clinical findings in hypocalcemia include:
serum calcium < 4.5 mEq/L
muscle spasms, twitching, cramping, tetany
positive Chvostek's sign
positive Trousseau's sign
tonic/clonic seizures
bradycardia, decreased cardiac contractility
cardiac dysrhytmias, arrest
altered blood clotting, bleeding (if Ca++ is very low)
hypotension
Management of hypocalcemia includes:
oral or intravenous calcium
give oral calcium 30 minutes before other meds/meals to aid absorption
encourage dietary intake of calcium, e.g. milk, cheese, broccoli
careful use of laxatives, antacids and phosphate enemas
monitor serum calcium, albumin and clotting levels
avoid hyperventilation/respiratory alkalosis
Causes of hypercalcemia include:
prolonged immobility
osteoporosis
excess calcium or vitamin D intake
indiscriminate use of antacids containing calcium
bone tumors and tumors of the lung, stomach, and kidney
hyperparathyroidism
hypophosphatemia
alkalosis
thyrotoxicosis (hyperactivity of the thyroid )
Addison's disease (adrenal insufficiency)
acute renal failure
prolonged use of thiazide diuretics
Hypercalcemia may be manifested by:
serum calcium level > 5.5 mEq/L
confusion, personality change, depression
pathologic fractures
lethargy, drowsiness, apathy
heart block or cardiac arrest with large excess of Ca++
increased cardiac contractility
digitalis toxicity
anorexia, nausea, vomiting, constipation
abdominal pain
polyuria, polydipsia
renal calculi accompanied by flank pain
hypertension
Management of hypercalcemia may include:
encourage weight bearing & physical activity if possible
loop diuretics may be used to increase urine output and Ca+ loss
corticosteroids
proper use of supplemental vitamins
encourage fluid intake
monitor cardiac function
phosphate binders
monitor for urinary calculi
treat malignancies, if present
hemodialysis
meds which inhibit bone resorption
Mg++ fun facts:
Mg++ is absorbed from food and lost via urine and stool.
About 1% is found in the ECF, 60% is in bone, and the remainder is in muscle and soft tissue. About one-third of Mg++ is bound to protein.Two-thirds of Mg++ is free in the plasma.
Magnesium is the second highest electrolyte in ICF concentration, second only to potassium.
Mg++ and ___are tied together in function, thus a deficiency of one affects the other.
The kidneys are the primary way magnesium is eliminated from the body; therefore, impaired renal function changes magnesium balance.
Ca++
What does Mg++ do?
affects skeletal muscles by depressing acetylcholine release at synaptic junctions
regulates neuromuscular irritability (excitability)
aids absorption of calcium from the intestine
aids calcium metabolism
affects parathyroid hormone secretion and therefore intracellular calcium
aids transport of potassium and sodium across cell membranes
is required for use of ATP (adenosine triphosphate) as a source of energy (thus, Na+ - K+ pump is affected by decreased Mg++)
activates enzymes which influence protein and nucleic acid synthesis
assists in cell metabolism
regulates ICF concentrations of potassium, calcium and phosphorus
aids blood clotting
Low serum magnesium (hypomagnesemia) levels may be caused by:
chronic alcoholism
uncontrolled diabetes mellitus
malabsorption syndromes
starvation
renal disease which causes excess excretion
impaired renal conservation of magnesium
bowel resection with ileostomy or colostomy
low calcium or potassium levels
hyper and hypoparathyroidism
hyperthyroidism
excessive loss of fluid from the gastrointestinal tract
vomiting and diarrhea
nasogastric suction
intestinal or biliary fistulas
ulcerative colitis
cirrhosis of the liver
prolonged TPN or intravenous fluids without adequate Mg++
primary aldosteronism, hyperaldosteronism
acute and chronic pancreatitis
treatment of diabetic ketoacidosis (Mg++ moves into cell with K+ after insulin administration)
Low serum magnesium (Hypomagnesemia) may be demonstrated by:
serum Mg+ < 1.5 mEq/L
hyperirritability, seizures
tetany, foot and leg cramps, hyperactive reflexes, tremors
paresthesia of the legs and feet
positive Chvostek's sign
vasodilation with hypotension, dizziness
confusion, hallucinations, delusions
insomnia, lethargy
dysrhythmias - tachycardia, premature ventricular contractions, ventricular fibrillation
electrocardiogram changes with mild or severe deficits
digitalis toxicity
nausea; vomiting, anorexia
low serum calcium and potassium
low serum calcium that does not improve after calcium gluconate
low urine Mg++
Hypomagnesemia can be managed by:
slow (to prevent cardiac arrest) intravenous infusion of magnesium sulfate
oral or intramuscular magnesium sulfate
dietary intake of Mg++ (if reduced food intake was the cause)
reduce auditory, visual, mechanical stimulation
monitoring cardiac and neurologic status
teaching the need to avoid abuse of antacids and laxatives
Hypermagnesemia may be caused by:
chronic renal failure; decreased renal function
excessive intake of magnesium, laxatives or antacids containing Mg++
adrenal insufficiency (Addison's disease)
aspiration of sea water
hyperparathyroidism
hypothyroidism
untreated diabetic ketoacidosis
dehydration
Hypermagnesemia may be manifested by:
serum Mg+ > 2.5 mEq/L
feeling of warmth and sweating accompanied by severe depression
bradycardia, weak pulse
electrocardiogram changes
prolonged QT interval
heart block
cardiac arrest (with very high Mg+ levels)
lethargy, drowsiness
confusion, coma
tremors, hyporeflexia
muscle weakness
flaccid paralysis, respiratory muscle paralysis
hypotension
The treatment of hypermagnesemia may include:
dialysis for the person who has renal failure
stop antacids and laxatives containing Mg++
calcium gluconate intravenously
encourage fluid intake to increase urinary excretion of Mg++
monitor cardiac and respiratory function
Which of the following assessment findings would you expect to see in hypermagnesemia?
decreased pulse and blood pressure
The normal serum level of chloride (Cl-) is ___ mEq/L.

Chloride is taken into the body via food and excreted by the kidneys.

Chloride is mainly in the ECF, with lesser amounts in the interstitial and intracellular fluids.

Chloride is found in gastrointestinal fluids.

Chloride concentration increases or decreases with changes in the concentration of other anions.

Chloride competes with bicarbonate to combine with sodium. If the chloride level drops, the serum bicarbonate level increases and vice versa.

If sodium is reabsorbed as a result of aldosterone action, there will be an increased reabsorption of chloride.
95-108
Functions of chloride include:
aiding cell integrity by influencing osmotic pressure
acid-base balance
water balance
Hypochloremia may be caused by
excessive hydrogen (H+) loss
prolonged use of 5% dextrose in water intravenous fluids
drugs such as:
bicarbonate
furosemide (Lasix)
thiazide diuretics
ethacrynic acid (Edecrin)
severe vomiting and diarrhea
excessive biliary, nasogastric or fistula drainage
acute infections
adrenal insufficiency (Addison's disease)
severe burns
metabolic alkalosis
heart failure
untreated diabetic ketoacidosis
heat exhaustion
fever
ulcerative colitis
Hypochloremia may be exhibitied by:
serum chloride level < 95 mEq/L
pH < 7.45 (metabolic alkalosis - kidneys respond to chloride drop by reabsorbing bicarbonate)
symptoms may be those associated with metabolic alkalosis
hyperirritability
tetany, hypertonic muscles
depressed respirations
low potassium and sodium, and the symptoms which accompany those deficits
The treatment for hypochloremia may include:
intravenous administration of sodium chloride
ammonium chloride
treat the cause
Hyperchloremia (excess serum chloride) may result from:
drop in ECF bicarbonate
excess intravenous sodium chloride
use of certain drugs
cholestyramine (Questran)
phenylbutazone (Butazolidin)
ammonium chloride
boric acid
ion exchange resins
hyperventilation
anemia
Cushing's syndrome
cardiac decompensation
primary hyperparathyroidism
metabolic acidosis (bicarbonate excreted, replaced with chloride)
respiratory alkalosis
Hyperchloremia may be exhibited by:
serum chloride level > 108 mEq/L
pH < 7.35 (metabolic acidosis), a drop in bicarbonate causes an increase in chloride
symptoms associated with metabolic acidosis
electrocardiogram changes
stupor, coma
deep, rapid breathing (Kussmaul breathing)
weakness
The management of hyperchloremia includes:
prevention
treat the cause
What would you find on assessment that would be consistent with low serum chloride?
pH > 7.45. A low serum chloride will be accompanied by an increase in bicarbonate.
Which one of the following would be an expected sign / symptom of hyperchloremia?
stupor, coma. Changes in levels of mental state would be a key indication of hyperchloremia.
Fun facts about P:
It is the most abundant anion (negative charge) in the ICF.

Phosphorus is regulated by the parathyroid hormone (PTH). PTH causes phosphorus to move from the bone to the plasma.

About 80-85% of the total phosphorus content in the body is combined with calcium in the bones and teeth, the rest is in the blood as phosphate or esters.

Phosphorus enters the cell with glucose and is lowered after carbohydrate ingestion.

Calcium and phosphorus levels are evaluated in relationship between the two. If calcium is reduced, phosphorus will be increased, and vice versa.

An excess in the serum level of calcium (or phosphorus) will cause the kidney to excrete the other.
Phosphorus is necessary for:
formation of bone
regulating the level of a substance in red blood cells which reduces the affinity of hemoglobin for oxygen
acid-base balance
storage and transfer of energy from one site to another
Hypophosphatemia (low serum phosphorus) may result from:
hyperparathyroidism (serum Ca++ will be elevated)
hyperinsulinism
continous administration of intravenous glucose (in non-diabetic)
treatment of diabetic ketoacidosis
prolonged respiratory alkalosis
excessive use of phosphate containing antacids
malabsorption syndromes
hyperalimentation with inadequate amounts of phosphorus
alcoholism
Findings in hypophosphatemia may include:
serum phosphate < 1.2 mEq/L
paresthesia (diminished or abnormal sensation.)
muscle weakness, tremors
ataxia (a staggering gait.), incoordination
disorientation, confusion, coma
seizures
long bone pain
shallow respirations
dysphagia
nystagmus (rapid,lateral eye movement.)
unequal pupils
The treatment of hypophosphatemia may include:
oral phosphate supplements (for mild to moderate deficiencies)
intravenous phosphate-containing solutions (for severe deficiency)
monitor serum calcium carefully
Hyperphosphatemia (excess serum phosphorus) may be caused by:
renal insufficiency or renal failure
hypoparathyroidism (with increased phosphorus, decreased calcium and normal renal function)
hypocalcemia
excessive intake of alkali (e.g. baking soda)
excessive intake of vitamin D
healing fractures
bone tumors
Addison's disease (adrenal hypofunction)
lymphomas
increased catabolism states
use of laxataives or enemas containing large amounts of phosphate
Excess phosphorus (hyperphosphatemia) may be manifested by:
serum phosphate > 3.0 mEq/L
cardiac dysrhythmias and muscle twitching (with rapid increase of phosphorus, the calcium drops, which affects muscles)
serum calcium < 4.5 mEq/L
tetany (short term)
soft tissue calcification (long term)
The management of hyperphosphatemia may include:
a thorough patient history to help find the cause
restrict dietary intake of phosphorus
give drugs which bind phosphate (certain antacids) if ordered
monitor serum calcium levels
observe for tetany and cardiac dysrhythmias
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