Nursing
63-273
ASSESSMENT & CARE OF CLIENT EXPERIENCING ELECTROLYTE IMBALANCE
See Table 16-18 Fluid and Electrolyte Imbalances p. 355 Lewis 6th ed.
Sodium (p. 338-342) Lewis 6th ed.
The most abundant electrolyte in the E.C.F., helps to control water distribution in the body,
primary regulator of extracellular fluid volume, a loss or gain of Na usually accompanied by loss
or gain of water, establishes the electrochemical state needed for muscle contraction and nerve
impulse transmission.
Normal value of serum Na - 135-145 mmol/l (S.I.units)
Behaviours Associated With Hyponatremia (Low sodium - less than 135 mmol./l.) Table 16-4
Water and Na Imbalances and Clinical Manifestations p. 339 Lewis 6th ed.

Nausea, abdominal cramping

Anorexia, muscle cramps and feelings of exhaustion (associated with Na loss and water
gain)

Levels less than 115 mmol./l. cause behaviours associated with I.C.P. - lethargy,
confusion, muscular twitching, focal weakness, hemiparesis, papilledema and seizures.
Stimuli Leading to Hyponatremia Second Level Assessment (Table 16-4 Lewis p. 339)
Na Loss

Vomiting, diarrhea, fistulas, sweating

Diuretics that decrease absorption of Na - e.g. Loop diuretics especially when combined
with a low salt diet

Adolesterone deficiency due to adrenal insufficiency.
Dilutional Hyponatremia

Water intoxication - the serum Na is diluted by an increase in the ratio of water to Na
causing ECF volume excess and an ICF volume excess

Stimuli causing this type are:

syndrome of inappropriate diuretic hormone or SIADH (excessive ADH activity
with water retention and dilutional hyponatremia, and inappropriate urinary
excretion of Na in the presence of hyponatremia - 100 mmol/l or less) caused by
Oat cell lung tumors, head injuries, endocrine/pulmonary disorders(pneumonia,
asthma, Tb, empyema and pneumothorax), use of medications such as pitocin,
cyclophosphamide, vincristine, thioridazine and amitriptyline

hyperglycemia-causes an osmotic gradient causing H2O to leave the cell and
move into the ECF

increased water intake through administration of electrolyte poor I.V. fluids such
as Dextrose and water

use of tap water (hypotonic) enema which moves into the ECF and causes
dilutional hyponatremia or irrigation of gastric tubes with water instead of saline
with same effect

compulsive water drinking (psychogenic polydipsia) - self-induced

T.U.R.P. syndrome - complication postop transurethral resection of the prostrate
gland - irrigation fluid is absorbed into the extracellular fluid producing
circulatory overload, pulmonary edema and hyponatremia - it is extremely
important to do strict intake and output with each bag of irrigating fluid hung to
determine that there is more output than input and that the irrigating fluid is not
being retained!
-2Interventions for Patients With Hyponatremia (Management of Stimuli) p.341 Lewis 6th
1. Identify those patients at risk for hyponatremia (i.e. with stimuli as those listed above)
2. Review medications that the patient is receiving that can predipose to hyponatremia.
3. Monitor:

fluid losses and gains for all patients at risk for hyponatremia. Look for loss Na
containing fluids (GI secretions/sweat) Monitor body weight since loss of 1 L. of
fluid = 0.9 kg. loss of wt.(approx 2 lbs)

lab values for serum sodium levels lower than normal

for presence of GI symptoms such as anorexia, nausea, vomiting and abdominal
cramping as these could be early signs

for CNS changes such as lethargy, muscular twitching, convulsions and coma,
which may come on rapidly due to water overloading.
4. Encourage foods and fluids with high Na content - e.g. beef broth made with one
cube contains 900 mg. of Na, 8 oz of tomato juice contains 700 mg. of Na, table salt, soy
sauce, pork and cheese are sodium rich
foods.
5. Use extreme caution when administering hypertonic saline solutions (3 or 5%) since
they can be lethal if administered carelessly. Use a volume controlled apparatus/I.V.
pump, check serum Na levels before and during treatment. Na levels should not be raised
too rapidly unless necessary to control cerebral edema. Monitor patients with heart
disease for signs of circulatory overload and pulmonary edema.
6. Avoid large water supplements to patients receiving isotonic tube feedings.
7. Ensure an adequate salt intake for all patients on lithium and monitor these patients
closely if they have sweating or diarrhea, as low Na decreases intolerance to lithium.
These patients should not take diuretics.
8. Patients with adrenal insufficiency should take steroids as prescribed, keep several days
dosage with them, increase dietary salt intake if excessive sweating or diarrhea occurs,
monitor intake and output.
9. If osmotic diuretics are given to increase excretion of water without sodium such as
mannitol/osmitrol, monitor patient for excessive fluid loss and low K levels.
10. Fluid restriction may be necessary in patients with renal disease.
-3Hypernatremia - Na Excess (greater than 145 mmol.l) (See Table 16-4 p.339 Lewis 6th ed.)
Behaviours Associated With Hypernatremia
neurologic and the result of cellular dehydration, often overlooked as reason for change in
behaviour in the elderly, children also high risk.
Early signs are lethargy, weakness and irritability.
Late signs are convulsions, extreme lethargy, stupor and coma - Level of consciousness depends
on rate of development

restlessness and weakness in moderate hypernatremia

disorientation, delusions and hallucinations in severe hypernatremia

brain damage due to subarachnoid hemorrhages from the brain contracting

thirst (such a strong defender of serum Na levels that hypernatremia never occurs in
normal person), only in unconscious or those with no access to water

ill people may have impaired thirst mechanism and are therefore at risk

dry, swollen tongue, sticky mucous membranes, flushed skin, peripheral and pulmonary

edema, postural hypotension, increased muscle tone and deep tendon reflexes

mild elevation in body temperature

urine specific gravity and urine osmolality is increased as the kidneys try to conserve

water (provided water loss is from a source other than the kidneys).
Stimuli Leading to Hypernatremia (Table 16-4 p. 339 Lewis 6th ed.)
Gain of Na in excess of water - I.V. administration of hypertonic saline(3-5%),
excessive use of sodium bicarbonate(used in cardiac arrest), increased ingestion of salt,
0.9% saline given in response to a loss which is primarily H2O
Loss of water in excess of Na - deprivation of water in unconscious patients who cannot
perceive thirst especially high risk ae very old, very young or cognitively impaired who
cannot communicate their thirst, administration of hypertonic tube feedings without
adequate water supplements, watery diarrhea, increased insensible water loss (as in
hyperventilation or burns), diabetes insipidus if patient cannot respond to thirst or liquids
are restricted, heatstroke, near drowning in sea water, malfunctioning of peritoneal or
hemodialysis proportioning systems.
Interventions for Patients With Hypernatremia (Management of Stimuli) (p. 340 Lewis 6th)
1. Identify patients at risk for hypernatremia (see stimuli above)
2. Monitor:

fluid losses and gains(1L. of fluid = 0.9 kg.)

for behaviours associated with hypernatremia (see above)

serum Na levels

patient's response to corrective parenteral fluids - neurologic signs should improve

I.V. solutions of glucose and water (5%)correction should be achieved over 48h
with IV therapy since rapid correction could lead to cerebral edema
3. Offer debilitated individuals fluids frequently to prevent hypernatremia and notify the
doctor stat if patient is unable to take fluids, so that they may be given by alternate route.
4. If tube feedings are used give sufficient fluids to maintain serum Na and BUN in
normal range.
5. Educate patients with regard to the proper use of medications and how to monitor I&O.
-4Health Teaching re: Prevention of Heat Disorders
1. Aclimatize to a hot environment before undergoing strenuous activity.
2. Drink at regular intervals while undergoing heat stress - not alcohol, coffee or tea due
to diuretic effect, water or electrolyte solutions.
3. Avoid strenuous activity on hot days.
4. Wear loose, porous clothing.
5. Increase sodium intake prior to athletic event, avoid fluid restriction poor to an event,
have frequent fluid stations, trained spotters at regular intervals, use buddy system. At
regular intervals, replace lost fluid with cold water.
Potassium("Star of the Cell") p.342 -345 Lewis 6th

the major intracellular electrolyte, influences both skeletal and cardiac muscle
activity, potassium moves in and out of the cells via the Na-K pump.

80% of potassium is excreted by the kidneys, 20% through bowel and sweat
glands

kidneys regulate amount of potassium that is excreted in the urine, concentration
gradient favours movement of potassium into the renal tubule to be excreted in the
urine, kidneys cannot serve K as well as they do Na and therefore may still excrete
K in the presence of potassium depletion.
Normal value of serum K - 3.5 to 5.5 mmol./l (S.I.)
Hypokalemia (K Deficit)
Behaviours Associated With Hypokalemia (See Table 16-6 Lewis 6th p. 343)

death through cardiac or respiratory arrest

level below 3 mmol./l

fatigue, anorexia, nausea, vomiting, muscle weakness, leg cramps decreased bowel
motility, paresthesias, dysrhythmias and increased sensitivity to digitalis

hypokalemia can lead to inability of the kidneys to concentrate urine, causing dilute

urine, polyuria, nocturia and excessive thirst, depresses the release of insulin and results
in glucose intolerance

ECG changes - flat T waves and depressed ST segment, presence of a U-wave (See ECG
changes assoc. with hypokalemia Fig. 16-14 Lewis p. 344)

can lead to alkalosis
-5Stimuli Leading to Hypokalemia (Table 16-6 p. 343 Lewis 6th)

GI loss of potassium most common cause - vomiting, gastric suction partly due to direct
loss in gastric fluid and also through the kidneys in response to metabolic alkalosis,

patients with bulemia, diarrhea, prolonged intestinal suctioning, recent ileostomy, villous
adenoma (a tumor of the intestinal tract characterized by excretion of potassium rich
mucous)

alkolosis can lead to hypokalemia - H+ ions move out of the cell in alkalotic states to help
correct the high pH and K+ions move into the cell to maintain an electrically neutral state
(hypokalemia can also cause alkalosis)

hyperaldosteronism increases loss of K by the kidneys as in patient with adrenal

adenomas or secondary to cirrhosis, nephrotic syndrome, CHF and malignant

hypertension

K losing diuretics eg. Furosemide/lasix and thiazides, ethnacrynic acid especially in large
doses in patients with low K intake, in patients with laxative abuse

corticosteroids, sodium penicillin, carbenicillin and amphotericin B

insulin hypersecretion since insulin promotes entry of K into skeletal muscle and
hepatic cells - eg. Patients on T.P.N. receiving high CHO parenteral fluidspatients with
inadequate nutrition for prolonged periods - eg. Debilitated elderly, alcoholics, and
patients with anorexia nervosa
Interventions for Patients with Hypokalemia (Managing the Stimuli) (p. 345 Lewis 6th)
1. Identify patients at risk for hypokalemia - see stimuli above.
2. Monitor

for behaviours associated with hypokalemia

digitalis toxicity in patients who are on digoxin & prone to low K

patients receiving I.V. potassium very carefully - must be diluted in the maximum

amount of fluid the patient can tolerate (KCl usually added to full bag of 1000 ml
of .9% NaCl to avoid glucose favouring a shift of K into the cells), potassium

levels should be increased gradually, E.C.G. should be monitored if increased
rapidly in emergency situations, ensure patient's urinary output is greater than 30
ml./hr since K is excreted through the kidneys, use an infusion pump, mix well in
the bag.
3. Prevent hypokalemia by: See Pt. and Family Teaching Guide Table 16-7 Prevention
of Hypokalemia p. 345

encouraging intake of K rich food and fluid eg. avocado, raisins, dried dates,
cantelope, bananas, baked potato, and orange juice

discourage abuse of diuretics/laxatives

educating patients regarding the use of salt substitutes which contain 50-60
meq.of potassium/tsp. Fine for patients on potassium losing diuretics but not for
those on potassium conserving diuretics such as spirolactone, triamterene
-6Hyperkalemia
Behaviours Associated With Hyperkalemia (lst Level Assessment) (Table 16-6 p.343 Lewis
6th)

cardiac effects with level above 6-8 mmol./l peaked narrow T waves, ST depression and

shortened QT interval, then prolonged PR interval and P waves disappear, can lead to
ventricular dysrhythmias and cardiac arrest(See ECG changes assoc. with hyperkalemia
Fig. 16-14 Lewis p. 344)

skeletal muscle weakness and even paralysis if severe deficit

GI such as nausea, intermittent intestinal colic, diarrhea in hyperkalemic patients

often occurs with metabolic acidosis.
Stimuli Leading to Hyperkalemia (Table 16-6 p.343 Lewis 6th)

decreased renal secretion of potassium as in renal failure

excessive intake of potassium supplement or K conserving diuretics or salt substitutes

(high in K)

hyperaldosteronism and Addison's disease since deficiency of adrenal corticosteroids

causes Na loss and K retention

rapid I.V. potassium admin

rapid transfusion of aged blood (since K level rises in it)

acidosis

extensive tissue damage eg. crushing injuries

malignant cell lysis after chemotherapy
Intervention in Patients With Hyperkalemia (See p.343-344 Lewis 6th)
1. Identify patients at risk for hyperkalemia - see stimuli above.
2. Prevent hyperkalemia by following guidelines for I.V. careful admin of K and safe
admin of potassium supplements, avoid administering potassium sparing diuretics, salt
substitutes and potassium supplements to patients with poor renal function, caution
patients to avoid foods high in potassium such as fruit, organ meats, pork, fish, beef,
chicken, and milk.
3. Collaborative interventions include measures to decrease K, such as stopping I.V.
admin, increase excretion with admin of lasix if renal function is good, give glucose
fluids with insulin I.V. to increase the uptake of K by cells and dilute the serum K.
*Administer ion exchange resins eg. Kayexalate orally or by enema (exchanges Na for K
in intestinal tract)
-7Calcium (p. 346 Lewis 6th ed.)

99% of the bodies calcium is in the skeletal system - component of bones and teeth

helps hold body cells together, 1% in the serum, possible to have osteoporosis yet

maintain a normal serum Ca level

sedative action on nerve cells, role in blood coagulation and acts as enzyme activator

helps regulate muscle contraction and relaxation incl. normal heart beat.
Normal Value of Serum CA - 2.1-2.6 mmol./l.
Behaviours Associated With Hypocalcemia (See Table 16-8 Lewis 6th p. 346)

tetany due to increased neural excitability, spontaneous discharges of both sensory and

motor fibres in peripheral nerves

tingling in the tips of the fingers, mouth and feet

spasms of the muscles of the extremities and face may occur with pain

Trousseau's sign - carpopedal spasm will occur due to ischemia to ulnar nerve when B.P.
cuff pumped to 20 mm. Hg (See p. 347 Fig. 16-15 Lewis 6th)

Chvostek's sign - twitching of facial nerve muscles when nerve is tapped 2 cm. anterior to
the ear lobe, just below the zygomatic arch (See p. 347 Lewis 6th Fig. 16-15)

seizures

mental changes - emotional depression, confusion, delirium and hallucinations

prolonged QT internal due to elongation of the ST segment on ECG

ionized Ca may not be decreased if serum albumin is decreased, only total serum Ca is

decreased

. formula can be used to calculate the corrected total serum Ca in patients with low
albumin (see p. 223-9th Ed. Brunner)
Stimuli Causing Hypocalcemia (See Table 16-8 Lewis 6th p. 346)

hypoparathyroidism especially surgical and also associated with radical neck dissection in
first 24-48 hours postop

massive administration of citrated blood - eg. Newborn transfusion due to combining of
citrate with Ca and removing it from circulation temporarily

common in pancreatitis due to Ca combining with fatty acids released by lipolysis

forming soaps or to excessive secretion of glucagon from the pancreas resulting in
increased secretion of calcitonin (a hormone that lowers serum Ca)

associated with hyerphosphatemia

inadequate Vitamin D, Mg. deficiency, medullary thryoid Ca, low serum albumin levels
(since Ca is bound to proteins in the blood), and alkalosis

medications eg. aluminum containing antacids, aminoglycocides, caffeine,
corticosteroids, phosphates, loop diuretics, isniazid.
-8Interventions for Hypocalcemia (p. 347 Lewis 6th ed.)
1. Identify patients at risk for hypocalcemia - see stimuli above.
2. Collaborataive interventions include administration of p.o. calcium supplements or if
severe per I.V. Give Vitamin D to increase Ca absorption, administration of drugs to
decrease excitability of nerve and muscles eg. Robaxin, valium or magnesium sulphate.
3. Encourage patients to increase dietary intake of Ca in cheese, milk, yogurt, rhubarb and
increase exposure to sunlight (Vitamin D).
Hypercalcemia
Behaviours Associated With Hypercalcemia (See Table 16-8 Lewis 6th p. 346)

serum calcium greater than 2.6 mmol./l.

neuromuscular excitability due to suppression of activity at myoneural junction

muscular weakness, incoordination, anorexia, nausea, vomiting and constipation

abdominal and bone pain

Na linked Ca reabsorption at the proximal tubule

abdominal distention and paralytic ileus if severe

severe thirst secondary to polyuria caused by high solute Ca load

increased acid and pepsin production leading to behaviours associated with gastric ulcer

mental confusion, slurred speech, lethargy, acute psychotic behaviour or coma

cardiac arrest if Ca excess severe

can aggravate digitalis toxicity
Stimuli Associated With Hypercalcemia (See Table 16-8 Lewis 6th p. 346)

malignant neoplastic diseases

hyperparathyroidism

secondary to immobility after multiple # trauma or extensive trauma paralysis

use of lithium, overuse of alkaline antacids

Vitamin A and D intoxication
-9Interventions for Hypercalcemia (p. 346 Lewis 6th ed.)
1. Follow orders to discontinue I.V., Ca, Vitamin D and Ca supplements p.o., and stop
thiazide diuretics, lasix is ordered and infusions of normal saline which both promote
excretion of Ca and drugs that inhibit Ca resorption from bone may be given eg:
Calcitonin.
2. Patients' ECG should be monitored closely.
Magnesium

next most abundant intracellular cation to potassium

activator of many intracellular enzymes systems

role in CHO and protein metabolism

acts directly to produce a sedative effect on the myoneural junction, likely by
inhibiting

acetylcholine and therefore important in neuromuscular function

increases the stimulus threshold in nerve fibres

acts peripherally to produce vasodilation decreasing peripheral resistance
Normal value of serum Mg - 0.80-1.2 mmol./l
Behaviours Associated With Hypomagnesemia

one-third of magnesium is bound to protein and 2/3 exist as free cations Mg2+,
therefore

like calcium levels should be assessed in combination with albumin levels

symptoms occur if level less than 0.5 mmol./l.

neuromuscular changes - hyperexcitability, muscular weakness and tremors, and
athetoid

movements i.e. slow, involuntary, twisting and writhing, tetany, generalized tonicclonic or focal seizures, laryngeal stridor, +ve Chvostek's and Trosseau's sign
(Fig. 16-15 p. 347)

cardiac dysrhythmias and PVC's, supraventricular tachycardia, and ventricular
fibrillation

increased susceptibility to digitalis toxicity

mood alterations - apathy, depression, apprehension or extreme agitation, ataxia,
dizziness, insomnia and confusion, delirium, delusion, frank psychosis and visual
hallucinations.
- 10 Stimuli Associated With Hypomagnesemia (Table 16-10 p. 349 Lewis)

critical illness, *alcoholism*, starvation, those receiving TPN

GI tract losses from NG tube, diarrhea or fistulas

intestinal resection or small bowel disease (since this is where Mg is absorbed)

medications - aminoglyserides, cyclosporin, cysplatin, diuretics, digitalis,
amphotericin and citrated blood

associated with diabetic ketoacidosis due to increased renal excretion and shifting
of Mg into cells due to insulin therapy
Interventions for Patients With Hypomagnesemia p. 349 Lewis 6th ed.
1. Collaborative interventions such as D/C of drugs contributing eg. Loop diuretics,
osmotic diuretics, administration of Magnesium Sulphate I.V. in severe cases
2. Encourage intake of food and fluid rich in magnesium such as spinach, tuna and
yogurt, whole grain cereals, leafy green vegetables, nuts and legumes, bananas, oranges.
Behaviours Associated With Hypermagnesemia

progressive as serum level increases

peripheral vasodilation with facial flushing, sense of warmth, tendency for hypotension,

nausea and vomiting, drowsiness, decreased deep tendon reflexes, muscle weakness,

more severe hypotension and bradycardia, loss of patellar reflex, respiratory

depression and arrest, cardiac arrest.
Stimuli for Hypermagnesemia (Table 16-10 p. 349)

acute and chronic renal failure

excess magnesium administration or excessive use of laxatives with magnesium

adrenal insufficiency

hemodialysis with hard water
- 11 -
Interventions for Hypermagnesemia
1. Collaborative - D/C oral and parenteral magnesium, give magnesium free I.V. fluids
if renal function is adequate, give loop diuretics such as lasix to increase secretion of
Mg., administer I.V. calcium if levels severe.
2. Avoid food and fluid high in magnesium such as meat, fish, nuts, vegetables and
whole grains, leafy greens, bananas, oranges.
Phosphate - Normal 0.8-1.5 mmol./l
Hypophosphatemia p. 348 Lewis 6th ed.
Behaviours
Neurologic - irritability, fatigue, weakness, numbness, paresthesias, confusion, seizures, coma
Stimuli
malnourished patients, anorexia nervosa, alcoholism, patients on TPN, hyperventilation, alcohol
withdrawal, diabetic acidosis, thermal burns, low Mg and K, hyperparathyroidism, respiratory
alkalosis due to shift of phosphorus into the cell
Hyperphosphatemia (See 347 Lewis 6th)
Behaviours
tetany, tingling in fingertips and mouth due to reciprocal relationship with Calcium - Calcium
leaves serum and hypocalcemia results
metastatic calcification - complication in soft tissue, joints and arteries which results when
calcium - magnesium product (calcium x magnesium) exceeds 70 mg/dl.
Stimuli
renal failure, chemotherapy, hypoparathyroidism, respiratory acidosis, high phosphate intake,
profound muscle necrosis, increased phosphorus absorption
Fluid Imbalances
Fluid Volume Deficit p.337
Behaviours associated with fluid volume deficit (See Table 16-4 Water deficit Lewis 6th)

acute weight loss

decreased skin turgor

oliguria

concentrated urine

postural hypotension

weak, rapid heart rate

flattened neck veins

increased temperature

decreased C.V.P.

cool, clammy skin related to peripheral vasoconstriction

thirst

anorexia

nausea

lassitude

muscle weakness

cramps

Lab. Data incl. BUN elevated over creatinine level by 10:1

Hct is greater than normal since RBC's are suspended in less plasma volume

serum electrolytes can be reduced or elevated depending on the type of loss

urine specific gravity is increased greater than 1.020 (healthy conservation of
water)
Stimuli Causing Fluid Deficit ( See Table 16-4 Lewis 6th ed.)

abnormal fluid losses such as those from vomiting, diarrhea, GI suctioning

sweating

decreased intake - nausea or inability to access fluids

diabetes insipidus

adrenal insufficiency

osmotic diuresis

hemorrhage

coma

third space shifts or the movement of fluid from the vascualr system into other
spaces (i.e. with edema formation in burns or ascites with liver dysfunction)
Prevention
1. Control fluid losses with antiemetics, antidiarrhead medications
2. Office fluids frequently to debilitated patient.
3. Let doctor know stat if patient not able to take fluids.
Intervention (p.341 Lewis 6th ed.)
1. Replace with p.o. fluids if possible when the deficit is not severe.
2. Hypotensive patient usually treated with isotonic solutions of 0.9% NaCl or lactated
Ringer's solution) to expand the plasma volume.
3. When patient is normotensive a hypotonic electrolyte solution such as 0.45% NaCl is
used to provide electrolytes and free water for renal excretion of metabolic wastes.
4. Strict intake and output, kidneys may decrease urine output to less than 30 ml/hr to
conserve water, as fluid volume is restored the urine output should increase, the B.P.
should increase as well as C.V.P.
5. Daily body weight should be done an acute weight loss of 0.5 kg represents a fluid loss
of approx. 500 ml.
6. Closely monitor V.S. be alert for a drop of systolic pressure of greater than 15 mm
when patient goes from lying to sitting position (orthostatic hypotension)or weak, rapid
pulse.
7. Assess skin turgor over the sternum, inner aspect of the high or forehead - not as valid
in elderly as in young patients due to decreased elasticity. See Brunner 9th edition p.210
- evaluating tongue turgor which is not affected by age is preferred - additional
longitudinal tongue furrows would be present in dehydration and the tongue would be
smaller
8. Offer mouth care frequently.
An isotonic solution is one that is the same concentration as blood - the serum osmolality
ranges from 280-295mOsm/kg. The osmolality of an IV solution is written on the IV bag
itself. (The patient's serum osmolality can be approximately calculated by doubling the
patients sodium value eg. If there Na is 140, their osmolality is likely normal ie. 280).
This will help you assess whether the patient's IV solution is an appropriate/safe
concentration or not depending on their problem.(See Characteristics of Common I.V.
Solutions Table 16-19 Lewis p. 357)
Fluid Volume Excess Table 16-4 p. 339 Lewis 6th ed.
Isotonic expansion of the ECF caused by the abnormal retention of water and Na in the
approximate proportions that they exist in the ECF, secondary to an increase in total Na content
which then leads to an increase in total body water.
Behaviours associated with fluid volume excess

acute weight gain

edema

distended jugular veins

crackles

elevated CVP

shortness of breath

increased B.P.

bounding pulse

cough
Lab data: decreased Hgb and Hct

decreased serum and urine osmolality

decreased urine Na

decreased urine specific gravity
Stimuli causing Fluid Volume Excess (Table 16-4 Lewis 6th p. 339)
1. Compromised regulatory systems - renal failure
2. CHF
3. Cirrhosis
4. Overzealous administration of Na containing fluids/excess ingestion of table salt
5. Prolonged corticosteroid therapy
6. Severe stress and Hyperaldosteronism aggravate FVE
7. T.U.R.P. syndrome - fluid from irrigant is absorbed - important to monitor output with
bladder irrigation
Prevention
1. Instruct patients re restricted Na diet
2. Have patient check out over the counter medications with physician since some contain
Na.
Interventions
1. D/C Na containing IV fluids
2. Administering diuretics (thiazide for moderate and loop diuretics for severe), with K
supplements to prevent hypokalemia, restricting fluids and Na, TED stockings, supine
positioning
3. Hemodialysis/peritoneal dialysis if renal function impaired
4. I&O, daily weight, Gain of 0.9 kg = 1L. of fluid gain
5. Assess breath sounds
6. Monitor dependent edema - can measure the circumference of the extremity
Edema can be localized or generalized
Generalized edema is called anasarca
Ascites - form of edema in the peritoneal cavity.
Pitting edema - in the extremities, tissue can be compressed to form a pit.
Pulmonary edema - fluid in the pulmonary tissue and alveoli.
Third-Spacing - shift of fluid to third space i.e. from the vascular to the interstitial space due
to increased plasma proteins, increased capillary permeability, or lymphatic blockage secondary
to trauma, inflammation or disease. This shift can be localized to a single area or organ or can be
widespread.
Stimuli

peritonitis

blocked lymphatics eg. Metastatic Ca

heart failure

low plasma protein as in liver disease, burns, malnutrition, inflammation

septic shock

allergic reactions

postoperatively immediately after surgery lasting 48-72 hours capillary
permeability increases in areas of inflammation or trauma leading to a decrease in
the B.C.O.P. ( blood colloidal osmotic pressure) and a shift of fluid into the
tissues. Patient intake is greater than output by as much as 3:1 and pt. may
experience wt. gain. It is extremely important to increase the plasma protein lost
to increase B.C.O.P. and to decrease fluid loss from the vascular system.
Hypovolemic shock can develop postoperatively. This is called the loss phase.

as the inflammation and trauma subside - capillaries repair themselves and
reabsorption from the tissues begins. The fluid shifts back into the bloodstream
and is excreted by the kidneys. At this time there is a marked increase in urine
output (200 ml/hr) and electrolyte values may be low due to dilutional effect of
increased blood volume.This is called the reabsorption phase.