Download NR 115 Exam 3 Review Solution Type Description Examples

NR 115 Exam 3 Review
Solution Type
Description
Examples
-Close to the same
Isotonic
Hypotonic
osmolarity as
serum/body fluids
-Fluids remain in the
intravascular
compartment, thus
expanding it.
-Risk of fluid volume
overload.
-Fluids that contain less
sodium concentration than
serum
-Fluids enter the body and
move from extracellular
space into cells. Causing
them to swell.
-Risk of cardiovascular
collapse from vascular fluid
depletion.
Can also cause increased
intracranial pressure from
fluid shifting into brain
cells.
Indicated Uses
-Hypovolemic and
0.9%
Normal
Saline
Hypertensive patients
-Client has had
excessive fluid loss due
to vomiting/diarrhea
D5W
Lactated
Ringers
Solution
0.45%
Normal
Saline
0.33%
Normal
Saline
-Used when the cells
are dehydrated
secondary to gastric
fluid loss (NG
suctioning)
D10W
Hypertonic
Colloids
-Solutions enter the
body and draw fluid
from the extracellular
space, causing cells to
shrink and the
extracellular space to
expand.
-Risk of fluid overload
and pulmonary edema;
use with caution in
patients with renal or
cardiac disease.
-Plasma extender
-Risk for increased
blood pressure,
dyspnea, and bounding
pulse (hypovalemia)
3% Normal
Saline
-Used in clients with
hyponatremia, SIADH
5% Normal
Saline
Albumin
Dextran
Hetastarch
--Used with
Hypovolemia
Considerations when administering IV Therapy


5% Dextrose in Water (D5W): This solution is a little sneaky. If you look up the osmolarity, it is 278,
which is isotonic. However, when it gets into the blood stream the dextrose is rapidly metabolized,
leaving only water (hypotonic). Therefore, although the osmolarity is isotonic, physiologically D5W is
hypotonic. Receiving D5W can lead to cerebral edema because of the movement of water from the
vascular system into the cells.
0.9% sodium chloride: Used to replace sodium and chloride and treat metabolic alkalosis. Use with
caution in patients who are at risk for fluid retention
Condition and
Etiology
Dehydration
(Hyperosmolar
Imbalance)
Etiology:
-Diabetes Insipidus
(brain fails to secrete
enough ADH)
-Interruption of
neurologically driven
thirst drive
-Administration of
hypertonic enteral tube
feedings
Description
Loss of Body Fluids →

Increased Blood
Solute
Concentration

Increased
Osmolality

Increased Serum
Sodium
Concentration
In an attempt to maintain
balance between
extracellular and
intracellular space:
Water in Cells →
Concentrated Blood
-This shift along with water
intake and fluid retention in
kidneys will lead to
restoration of body fluid
volume.
-Without adequate water
intake, fluid continues to
move out of the cells into
the extracellular space,
leading to cell shrinkage
and malfunctioning
Physical
Assessment
Findings
Diagnostic
Laboratory
Findings
Etiology:
-Hemorrhaging
-Excessive diuretic
therapy
-Excessive
perspiration
-Vomiting and diarrhea
Dry and Sticky
Mucous Membranes
Thirst
Increased Body
Temperature
Increased serum
sodium level > 145
mEq/L
Increased serum
osmolality level ( >
300 mOsm/kg
Change in Mental
Status
Increased HCT
Convulsions, Coma
Urine specific gravity
> 1.030
Accurate I & O
If patient can
handle oral fluids,
encourage them
Severe cases administration of
hypotonic solution
Monitor IV
infusions,assess for
complications
Monitor serum sodium,
urine osmolality and
urine specific gravity
Seizure precaution
Daily weights
Replace lost fluids
with isotonic fluids
--> expand
circulating volume
Tachycardia
Vary depending on
the underlying cause
Dry mucous
membranes
Urine specific gravity
> 1.030
Blood transfusion
Weak pulse
Increased HCT
levels (>%50)
Dopamine
(Vasopressor)
Albumin infusion
Refers to isotonic fluid loss
from the extracellular space
Nursing
Interventions
Monitor s/s and vital
signs closely
Postural hypotension
Fluid Volume
Deficit
Treatment
Lower HOB slow a
declining BP
Monitor VS frequently
Maintain and monitor IV
infusion
Assess mental status
Oliguria
Oxygen therapy -> tissue perfusion
Assess peripheral
pulses and skin
temperature
Monitor urinary output
(hourly)
Condition and
Etiology
Description
Physical
Assessment
Findings
Diagnostic
Laboratory
Findings
Treatment
Nursing
Interventions
Assessment of VS
very closely, BP and
respiratory changes
Hypervolemia
(Fluid Volume
Excess)
Etiology:
-CHF
-Renal Failure
-Cirrhosis of the liver
-Excessive sodium or
fluid intake, retention, or
a shift in fluid from the
interstitial space into the
intravascular space.
-IV replacement therapy
with an isotonic solution
-Blood replacement
Assessment for
distention of vein in the
hands or neck
Edema especially in
dependent areas
Excess of isotonic fluid
in the extracellular
compartment.
Osmolality is usually
unaffected because fluid
and solutes are gained
in equal proportion.
The body has
compensatory
mechanisms to deal with
hypervolemia, but when
they fail, signs and
symptoms of
hypervolemia develop.
Hypertension
Decreased HCT level
< 38% due to
hemodilution
Crackles in lungs
Confusion
Neck vein distention
Decreased serum
osmolality
Pulmonary congestion
on CXR
I & O hourly
Restriction of
sodium and fluid
intake
Diuretic therapy
Assessment of breath
sounds
Raise HOB to help the
client breathe easier
Oxygen therapy
Monitor restriction of
fluids
Weight gain usually
rapid
Assess response to
diuretic therapy
Check for a S3 audible
heart sound - happens
when the ventricles
are overloaded
Daily weights and
evaluate trends
Hypoosmolar
Imbalance
(Water
Intoxication)
Etiology:
-SIADH secondary to
CNS or pulmonary
disorders, head trauma,
certain medications and
some surgeries
-Also seen with rapid
infusion of hypotonic
solution
Excessive use of tap
water as a nasogastric
tube irrigant or tap water
enema
Occurs when excess
fluid moves from the
extracellular space to
the intracellular space.
Excessive low-sodium
fluid in the extracellular
space is hypotonic to the
cells; the cells are
hypertonic to the fluid.
Because of this
imbalance, fluid shifts by
osmosis into the cells
which have
comparatively less fluid
and more solutes.
That fluid shift, which
causes the cells to swell,
occurs as a means of
balancing the
concentration of fluid
between the two spaces,
a condition called water
intoxication.
HA's, personality
changes, LOC
changes such as
confusion, irritability,
or lethargy
Nausea, vomiting,
cramping, muscle
weakness, twitch,
thirst, dyspnea on
exertion
Low sodium levels
Serum osmolailty <
280 mOsm/kg
Restrict PO and
Parenteral fluid
intake
Severe cases hypertonic
solutions to draw
fluid out of the
cells
Note the cause,
and correct the
underlying cause
Prevention
Neurological status
closely monitored
Monitor VS
Accurate I & O
Maintain fluid
restrictions
Weigh daily
Monitor serum lab
values
Provide safe
environment, seizure
precaution
Electrolytle Imbalances (The Short Version)
 Sodium - body water balance


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

Potassium - contraction of skeletal and smooth muscle and nerve impulse conduction
Calcium - formation and structure of bones and teeth, cell structure and function, cell membrane permeability and impulse
transmission, the contraction of all muscle types and is necessary in the blood clotting process
Chloride - important in the digestive acids; closely linked to sodium
Magnesium - affects nerve and muscle action by affecting calcium usage, activates enzymes involved in carbohydrate and
protein metabolism, helps in the transport of sodium and potassium across cell membranes, and influences the levels of
sodium, potassium, calcium and some body hormones (parathyroid hormone)
Phosphorus - formation and structure of bones and teeth, this electrolyte is needed in the following activities: utilization of B
vitamins, acid base homeostasis, bone formation, nerve and muscle activity, cell division, the transmission of hereditary
traits, metabolism of carbohydrates, proteins and fats
Sodium Imbalances
 Sodium is one of the most important elements in the body. It accounts for 90% of extracellular fluid
cations, and is the most abundant solute in extracellular fluid.
 Sodium levels are a good indicator of hydration; a high sodium means dehydration, and a low sodium
means FVE or water excess
 Sodium is found in the extracellular fluid
 Sodium is excreted through the GI tract and in sweat.
Hyponatremia:
o
o





Sodium deficiency where body fluids are diluted and cells swell from decreased extracellular fluid osmolality
Can lead to seizures, coma, and permanent neurologic damage
Initial s/s
o Nausea and malaise
As water shifts from the extracellular fluid space to the intracellular fluid space brain cells swell, causing progressive
neurologic signs and symptoms, including:
o Headache
o Lethargy
o Confusion
o Coma
Major signs of hypernatremia are neurologic:
o Altered mental status
o Neuromuscular irritability
o Weakness
o Focal neurologic deficits
o Seizures and coma
Treatment
Treatment guided by the underlying cause
o If volume depleted, Give isotonic infusions
o Volume overload, Treat with fluid restriction and diuretics
o If symptoms of hyponatremia are severe: Administer hypertonic saline
Hypernatremia: excess of sodium, less often seen. Can lead to seizures, coma and permanent neurologic damage.
-Thirst is the body's main defense against hypernatremia. Drive to respond to thirst is so strong that only people who can't
drink voluntarily such as infants confused elderly patients, or unconscious patients
Potassium Imbalances: diseases, injuries, medications, can all disturb potassium levels, must be ingested daily
as the body can't conserve it
MAGNESIUM IMBALANCES: Vital to neuromuscular system it affects contractility of cardiac and skeletal muscle. It
influences the body's calcium level through its effect on parathyroid hormone (PTH)

GI and urinary systems regulate magnesium through absorption, excretion, and retention. The body adjusts to any change in
the magnesium level. If level decreases, GI tract will absorb more magnesium and if level rises, the GI tract will excrete
through the feces
HYPOCALEMIA

Results from illness which directly affect the thyroid and parathyroid glands, or due to renal
insufficiency because the kidneys inability to excrete phosphorus
Phosphate Imbalances:






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Normal serum phosphate levels range from 2.5 - 4.5 mg/dL
Newborns have almost twice the adult level
Phosphorus is the primary anion of intracellular fluid
85% is combined with calcium in the teeth and bones, and skeletal muscle
Calcium and phosphorus exist in a reciprocal balance
Major function - muscle, RBC, and nervous system
Plays a role in CHO, fats, and protein metabolism
Hypophosphatemia is usually the result of inadequate dietary intake; it’s often related to malnutrition resulting from a prolonged
catabolic state or chronic alcoholism. Other causes include chronic use of antacids containing aluminum hydroxide, use of parenteral
nutrition solution with inadequate phosphate content, renal tubular defects, tissue damage in which phosphorus is released by injured
cells, and diabetic acidosis.
Symptoms: Hypophosphatemia produces anorexia, muscle weakness, tremor, paresthesia and, when persistent, osteomalacia,
causing bone pain. Impaired red blood cell functions may occur in hypophosphatemia due to alterations in oxyhemoglobin
dissociation, which may result in peripheral hypoxia. Hyperphosphatemia usually remains asymptomatic unless it results in
hypocalcemia, with tetany and seizures.
Hyperphosphatemia is generally secondary to hypocalcemia, hypervitaminosis D, hypoparathyroidism, or renal failure (often due to
stress or injury). It may also result from overuse of laxatives with phosphates or phosphate enemas.
Acid-Base Balance
Chemical buffers
– Carbonic acid-bicarbonate buffer system
Biological buffers
– Potassium (K+) shift
– Chloride (Cl-) shift
– Hemoglobin-oxyhemoglobin system
Physiological buffers
– Respiratory system
– Renal system
• Acidosis – pH < 7.35
– Caused by an excess of CO2 or H+ ions in
bloodstream or a deficit of HCO3 in the blood
stream
• Alkalosis – pH > 7.45
– Caused by an excess of HCO3 in the
bloodstream
or a deficit of H+ ions in the blood stream
Compensation will be manifested in opposite
physiological system
If cause is respiratory
• Compensation is metabolic (renal)
If cause is metabolic
• Compensation is respiratory
Respiratory acidosis:

Uncompensated (PCO2 >45 mm Hg; pH <7.4)

Impaired gas exchange or lung ventilation (chronic bronchitis, cystic fibrosis, emphysema): Increased airway
resistance and decreased expiratory air flow, leading to retention of carbon dioxide.

Rapid, shallow breathing: Tidal volume markedly reduced.

Narcotic or barbiturate overdose or injury to the brain stem: depression of respiratory centers, resulting in
hypoventilation and respiratory arrest.
Metabolic acidosis:

Uncompensated (uncorrected) HCO3- < 22 mEq/L; pH < 7.4

Severe diarrhea: Bicarbonate-rich intestinal (and pancreatic) secretions rushed through
digestive tract before their solutes can be reabsorbed; bicarbonate ions are replaced by renal
mechanisms that generate new bicarbonate ions.
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
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Renal disease: failure of the kidneys to rid body of acids formed by normal metabolic
processes.
Untreated diabetes mellitus: lack of insulin or inability of tissue cells to respond to insulin,
resulting in inability to use glucose; fats are used as primary energy fuel, and ketoacidosis occurs.
Starvation: Lack of dietary nutrients for cellular fuels, body proteins and fat reserves are used
for energy—both yield acidic metabolites as they are broken down for energy.
High ECF potassium concentrations: Potassium ions compete with H+ for secretion in
renal tubules; when ECF levels of K+ are high, H+ secretion is inhibited.
Respiratory alkalosis:

Uncompensated (PCO2 < 35 mm
Hg; pH > 7.4)

Direct cause
is always hyperventilation:
hyperventilation is pain/anxiety,
asthma, pneumonia, and at high
altitude represents effort to raise
PO2 at the expense of excessive
carbon dioxide excretion.

Brain injury or
tumor: abnormality of
respiratory controls.
Metabolic alkalosis:

Uncompensated (HCO3- >26 mEq/L; pH > 7.4)

Vomiting or gastric suctioning: loss of stomach HCl requires that H+ be withdrawn from blood to replace stomach
acids; thus H+ decreases and HCO3-proportionally.

Selected diuretics: cause K+ depletion and H2O loss. Low K+ directly stimulates the tubule cells to secrete
H+. Reduced blood volume elicits the renin-angiotensin mechanism, which stimulates Na+ reabsorption and H+ secretion.

Ingestion of excessive sodium bicarbonate (antacid): bicarbonate moves easily into ECF, where it enhances natural
alkaline reserve.

Constipation: prolonged retention of feces, resulting in increased amounts of HCO 3- being reabsorbed.

Excessive aldosterone: (adrenal tumors) promotes excessive reabsorption of Na +, which pulls increased amount of
H+ into urine. Hypovolemia promotes the same relative effect because aldosterone secretion is increased to enhance Na + (and
H2O) reabsorption.
1.
Note the pH. This tells you whether the person is in acidosis (pH < 7.35) or alkalosis (pH > 7.45); but it
does not tell you the cause.
2.
Next, check the PCO2 to see if this is the cause of the acid-base imbalance. Because the respiratory
system is a fast-acting system, an excessively high or low PCO2 may indicate either that the condition is
respiratory system—caused or that the respiratory system is compensating. For example, if the pH indicates
acidosis and:
A.
The PCO2 is over 45 mm Hg, the respiratory system is the cause of the problem and the condition
is a respiratory acidosis.
B.
The PCO2 is below normal limits (below 35 mmHg), the respiratory system is not thecause but is
compensating.
C.
The PCO2 is within normal limits; the condition is neither caused nor compensatedby the
respiratory system.
3.
Check the bicarbonate level. If step 2 proves that the respiratory system is not responsible for the
imbalance, then the condition is metabolic and should be reflected in increased or decreased bicarbonate
levels. Metabolic acidosis is indicated by HCO3-values below 22 mEq/L, and metabolic alkalosis by values
over 26 mEq/L. Notice that whereas PCO2 vary inversely with blood pH (PCO2 rises as blood pH falls), HCO3levels vary directly with blood pH (increased HCO3- results in increased pH). Beyond this bare-bones
approach there is something else to consider when you are assessing acid-base problems. If an imbalance
is fully compensated, the pH may be normal even when the pH is normal, carefully scrutinize the PCO2 or
HCO3- values for clues to what imbalance may be occurring.
Interpreting ABGs
Step 1. Use pH to determine Acidosis or Alkalosis.
< 7.35
Acidosis
ph
7.35-7.45
Normal or
Compensated
> 7.45
Alkalosis
Step 2. Use PaCO2 to determine respiratory effect.
PaCO2
< 35



35 -45
Tends toward
alkalosis
Normal
Causes high
or
pH
Neutralizes
Compensated
low pH
> 45



Tends toward
acidosis
Causes low
pH
Neutralizes
high pH
Step 3. Assume metabolic cause when respiratory is ruled out.

You'll be right most of the time if you remember this simple table:
High pH
Low pH
Alkalosis
Acidosis
High
Low PaCO2 High PaCO2 Low PaCO2
PaCO2
Metabolic Respiratory Respiratory Metabolic

If PaCO2 is abnormal and pH is normal, it indicates compensation.
o pH > 7.4 would be a compensated alkalosis.
o pH < 7.4 would be a compensated acidosis.
These steps will make more sense if we apply them to actual ABG values. Click here to interpret
some ABG values using these steps. You may want to refer back to these steps (click on "linked"
steps or use "BACK" button on your browser) or print out this page for reference.
Step 4. Use HC03 to verify metabolic effect

Normal HCO3- is 22-26
Please note:

Remember, the first three steps apply to the majority of cases, but do not take into account:
o the possibility of complete compensation, but those cases are usually less serious, and
o instances of combined respiratory and metabolic imbalance, but those cases are pretty
rare.
 "Combined" disturbance means HCO3- alters the pH in the same direction as
the PaCO2.
 High PaCO2 and low HCO3- (acidosis) or
 Low PaCO2 and high HCO3- (alkalosis).