CHAPTER 13: Fluid and Electrolytes: Balance
and Disturbance
→ important key terms
Acidosis: an increase in H+ concentration. Decreased
blood pH.
Metabolic acidosis: A low arterial PH due to reduced
bicarb concentration
Respiratory acidosis: low arterial pH due to increased
PCO2
Osmosis: the process by which fluid moves across a
semipermeable membrane from an area of low solute
concentration to an area of high solute concentration;
the process continues until the solute concentrations are
equal on both sides of the membrane
Ascites: edema in which fluid accumulates in the
peritoneal cavity
Hypertonic solution: a solution with an osmolality
higher than that of serum
Active transport: physiologic pump that moves fluid
from an area of lower concentration to a higher
concentration; requires ATP for energy
Hypotonic solution: a solution with an osmolality lower
than that of serum
Alkalosis: reduction of H+ concentration. Increased
blood pH.
Metabolic alkalosis: high arterial pH with increased
bicarb concentration
Respiratory alkalosis: a high arterial pH due to
reduced PCO2
Osmolality: the number of millimoles per kg of solvent
(mOsm/kg); used to evaluate serum and urine
Diffusion: the process by which solutes move from an
higher of higher concentration to a lower one, no
energy needed
Osmolarity: the number of millimoles per liter of
solution (mOsm/L); describes the concentration of
solutes or dissolved particles
Homeostasis: maintenance of a constant internal
equilibrium in a biologic system that involves positive
and negative feedback systems
Isotonic solution: a solution with the same osmolality
as serum and other body fluids
Hydrostatic pressure: the pressure created by the
weight of fluid against the wall that contains it. In the
body, hydrostatic pressure in blood vessels results from
the weight of fluid itself and the force resulting from
cardiac contraction
Tonicity: fluid tension or the effect that osmotic
pressure of a solution with impermeable solutes exerts
on cell size because of water movement across the cell
membrane
➢ Amount and composition of body fluids
○ 60% of typical adult’s weight consists of fluid (water and electrolytes).
○ Factors that influence: age, gender, body fat
○ People who are obese have less bodily fluid because fat cells contain less water
○ Intracellular space (ICF): fluid in the cells, takes up two thirds of the body fluid
and located primarily in skeletal muscle mass
○ Extracellular space (ECF): one third of the body fluid
■ Intravascular: fluid within the blood vessels; contain plasma, the effective
circulating volume. 3L blood volume is made of plasma, other 3L is
leukocytes, erythrocytes, thrombocytes
■ Interstitial: contains the fluid that surrounds the cells and totals about
11-12L in an adult, Lymph is here
■ Transcellular: 1L; transcellular fluids such as cerebrospinal, pericardial,
synovial, intraocular, pleural fluids, sweat and digestive secretions
○ Third space fluid shift or third spacing: loss of fluid into a space that does not
contribute to equilibrium. Early evidence in this is decrease in urine output des[ite
adequate fluid intake.
■ Urine output decreases because fluid shifts out of the intravascular space,
the kidneys then receive less blood and attempt to compensate by
decreasing urine output.
■ FVD which is intravascular fluid volume deficit: increased HR and body
weight, decreased BP and central venous pressure, and imbalances in fluid
intake and output
■ Can lead to… intestinal obstruction, pancreatitis, crushing traumatic
injuries, bleeding, peritonitis, and major venous obstruction
➢ Electrolytes
○ Most accessible way to measure electrolytes is the ECF plasma.
○ Sodium ions are most prevalent in the ECF because it affects the overall
concentration. It is important in regulating the volume of the body fluid
○ ICF’s major electrolytes are potassium and phosphate. ECF has low concentration
of potassium so it can only tolerate small changes.
■ The release of large stores of intracellular potassium, typically caused by
trauma to the cells and tissues can be extremely dangerous.
○ Hydrostatic pressure: is needed for the electrolyte movement. This is the normal
movement of fluids through the capillary wall into the tissues.
Sodium *
135- 145 mEq/L
Potassium *
3.5-5.0 mEq/L
chloride
98-106 mEq/L
Bicarbonate (HCO3) *
22-26 mEq/L
Calcium *
8.5-10.5 mg/dL
phosphorous
2.5-4.5 mg/dL
magnesium
1.8- 3.0 mg/dL
➢ Regulation of body fluid compartments
○ Osmosis and osmolality:
■ Osmosis: low to high concentration; the magnitude of this force depends
on the number of particles dissolved in the solutions, not on their weights
■ Osmolality: the number of dissolved particles contained in a unit of fluid
which determines and influences the movement of fluid between the fluid
compartments.
■ Tonicity: the ability of all solutes to cause an osmotic driving force that
promotes water movement from one compartment to another. The control
of tonicity determines the normal state of cellular hydration and cell size
■ Osmoles: sodium, mannitol, glucose, sorbitol (capable of affecting water
movement)
■ Osmotic pressure: the amount of hydrostatic pressure needed to stop the
flow of water by osmosis. It is primarily determined by the concentration
of solutes
■ Oncotic pressure: osmotic pressure exerted by proteins such as albumin
■ Osmotic diuresis: the increase in urine output caused by the excretion of
substances such as glucose, mannitol or contrast agents in the urine
○ Diffusion: the natural tendency of a substance to move from an area of higher
concentration to low concentration. Occurs through random movements of ions
and molecules
○ Filtration: movement of water and occurs from an area of high hydrostatic
pressure to an area of low hydrostatic pressure to an area of low hydrostatic
pressure
■ Examples: kidney filtration
○ Sodium- potassium pump: the sodium concentration is greater in the ECF than in
the ICF, because of this sodium tends to enter the cell by diffusion. This tendency
is offset by the sodium potassium pump that is maintained by the cell membrane
and actively moves sodium from the cell into the ECF. conversely the high
intracellular potassium concentration is maintained by pumping potassium into
the cell
➢ Systemic routes of gain and losses
Kidneys: regular urine output is 1-2L
Lungs: eliminate water vapor insensible loss at a
rate of approximately 300mL per day
Skin: sensible perspiration refers to visible water
and electrolyte loss through the skin (sweating),
can vary from 0-1000 mL or more every hour
depending on environment temp. Insensible
perspiration is continuous water loss by
evaporation (500mL/day). Fever and exercise
greatly increase water loss through lungs and the
skin as does the loss of natural skin barrier(burns).
GI tract: 100mL-200mL daily
➢ Lab test for evaluating fluid status
○ Osmolality: the concentration of fluid that affects the movement of water between
fluid compartments by osmosis measures the solutes(stuff) in urine and blood.
■ Blood: BUN (blood urea nitrogen) and glucose
■ Urine: urea, creatinine, uric acid
■ Normal: is 275-290 mOsm/kg
○ Osmolarity: normal is 10 mOsm/L
■ Urine specific gravity: 1010- 1025 is measure the kidney’s ability to
excrete or conserve water.
■ BUN: normal range is 10-20 mg/dL
● Increase: decreased renal function, GI bleeding, dehydration,
increased protein intake, fever, and sepsis.
● Decrease: end stage liver disease, low protein diet, starvation, any
condition that expands fluid volume (EX: pregnancy)
■ Creatinine: 0.7-1.4 mg/dL
■ Hematocrit: volume percentage of RBCs in the blood; 42-52% for men,
47% for women
➢ Gerontologic considerations
○ Normal physiologic changes of aging, which include reduced cardiac, renal, and
respiratory function and reserve and alterations in the ratio of body fluids to
muscle mass, may alter older adults’ responses to fluid and electrolyte changes
and acid base disturbances.
■ Respiratory: impaired pH
■ Renal: function declines with age, as do muscle mass, and daily
exogenous creatinine production. Therefore high normal and minimally
elevated serum creatinine
○ Medications
○ Dehydration which is the rapid loss of body weight owing to the loss of either
water or sodium. Which results in the increase of sodium concentration.
➢ Fluid volume disturbances
○ Hypovolemia
■ FVD occurs when loss of ECF volume exceeds the intake of fluid. It
occurs when water and electrolytes are lost in the same proportion as they
exist in normal body fluids; thus, the ratio of serum electrolytes remain the
same. May occur alone or with other imbalances.
Pathophysiology: decrease or inadequate fluid
intake
- Cause of fluid loss: vomiting,
diarrhea, GI suctioning, sweating
- Decreased intake: nausea, lack of
access, third space fluid shifts,
movement of fluid from vascular
system to other body spaces (EX:
ascites and edema)
- Diabetes insipidus, adrenal
insufficiency, osmotic diuresis,
hemorrhage, and coma
Gerontologic considerations: skin turgor is
used to assess for FVD but in the elderly
population it is not as accurate due to normal
loss of elasticity in the skin.
- Perform a functional assessment of
the older patient’s ability to
determine fluid and food needs and
adequate intake (aka do they need
help)
- Self conscious due to incontinence so
they may refrain.
Clinical manifestations: acute weight loss,
decreased BP, dizziness, weakness, thirst and
confusion, elevated pulse and temp, cool skin,
oliguric
Medical management: first line choice is
isotonic electrolyte solutions because they
expand plasma volume EX: 0.9% sodium
chloride and lactated ringer solution
As soon as the patient becomes normotensive,
a hypotonic electrolyte solution to provide
both electrolytes and water for renal excretion
of metabolic wastes
Assessment & diagnostic findings: elevated
BUN of 20:, hematocrit, creatinine, urine
specific gravity and osmolality, decrease in
urine sodium
Nursing management: monitor and measure
fluid I&O every 8 hours and sometimes every
hour, VS, skin and tongue turgor, urine
concentration, and mental function
○ Hypervolemia
■ FVE: fluid volume excess, isotonic expansion of the ECF caused by the
abnormal retention of water and sodium in approximately the same
proportions in which they normally exist in the ECF.
■ Edema is a common manifestation
● Ascites: fluid accumulates in the peritoneal cavity, it results from
nephrotic syndrome, cirrhosis and some malignant tumors
ALWAYS REPORTS SOB.
Pathophysiology: may be related to simple
fluid overload or diminished function of the
homeostatic mechanisms responsible for
regulating fluid balance
- Contributing factors: heart failure,
kidney injury, and cirrhosis of the
liver
- Excessive sodium containing fluids
Nursing management: I&O to identify
excessive fluid retention, weighed, breath
sounds, check for edema
- Edema: pitting you press a finger to
the affected part, creating a pit or
indentation that is evaluated on a
scale of 1+ minimal and 4+ severe,
peripheral which you measure the
circumference of the extremity with a
tape in millimeters
Clinical manifestations: peripheral ascites and
edema, distended neck veins, crackles, acute
weight gain, elevated CVP, SOB, increased
BP, respiratory rate, and urine output,
bounding pulse
Educating patients: low sodium diet, avoid
OTC meds without checking, promote rest,
monitor parenteral (IV) fluid therapy,
administer appropriate meds. If dyspnea or
orthopnea is present then you put the patient
in Semi Fowler’s position
Medical management: discontinue IV sodium
containing fluids, administer diuretics, restrict
fluids and sodium.
- Pharmacologic: mild to moderate
cases you use thiazide diuretics
which block sodium reabsorption in
the distal tube (EX:
hydrochlorothiazide, Microzide);
severe cases you give loop diuretics
they block the sodium reabsorption in
the ascending limb of Henle loop
Assessment and diagnostic findings: decrease
in all lab values: hemoglobin and hematocrit,
serum and urine osmolality, urine sodium and
specific gravity
-
-
EX: furosemide (Lasix)
Side effects: electrolyte imbalances
- hypo/hyperkalemia,
hyponatremia,
hyperuricemia
- Azotemia (increased
nitrogen)
Hemodialysis or peritoneal dialysis
may be used to remove nitrogenous
wastes and control potassium and
acid base balance and to remove
sodium and fluid
➢ Electrolyte imbalances
○ Most abundant in the ECF ranges from 135-145 is the determinant of ECF
volume osmolality.
○ Regulated by ADH, thirst, and the renin- angiotensin- aldosterone
○ Sodium functions in establishing the electrochemical states necessary for muscle
contraction and the transmission of nerve impulses
○ Inappropriate secretion of ADH, older patients are more at risk due to acquired
AIDS, those on mechanical ventilation, and people taking SSRIs
○ Sodium ( hyponatremia and hypernatremia)
○ Hyponatremia
■ Serum sodium level that is less than 135
■ Acute: commonly the result of a fluid overload in a surgical patient
■ Chronic: less serious neurological sequelae, outside hospital setting
■ Exercise associated hyponatremia, commonly found in women and those
of smaller stature. It can occur during extreme temperatures, because of
excessive fluid intake before exercise, or prolonged exercise that results in
a decrease in serum sodium
Pathophysiology: imbalance of water rather than
sodium. Urine sodium value assists in differing
renal and nonrenal causes.
- Low urine sodium: the kidney retain
sodium to compensate for non renal fluid
loss (vomiting, diarrhea, sweating)
- High urine sodium: renal salt wasting
(diuretic use)
- Dilutional, ECF volume is increased
without any edema
- Predisposed if you are deficient in
aldosterone, using meds such as
anticonvulsant, levetiracetam, SSRIs, or
desmopressin acetate
Medical management: focus on clinical symptoms
and lab values. GENERAL RULE, TREAT THE
UNDERLYING CONDITION
- Treatment: careful administration of
sodium by mouth, nasogastric tube or
parenteral route. Usually normal
consumption, if you cannot consume
regularly use lactated ringer solution or
isotonic saline.
- You cannot increase more than 12 in 24
hours to avoid neurologic damage due to
demyelination
- Altered cognition and decreased
alertness, ataxia, paraparesis
dysarthria, horizontal gaze
paralysis, pseudobulbar palsy,
and coma
- Restrict fluid
Clinical manifestations: poor skin turgor, dry
mucosa, headache, decreased saliva production,
orthostatic fall in BP, nausea, vomiting, and
abdominal cramping.
- Neuro: altered mental status, status
epilepticus and coma are related to
cellular swelling and cerebral edema.
- Anorexia, muscle abdominal cramps,
exhaustion
- Acute is worse than chronic because acute
decreases in sodium, developing in less
than 48 hours, may be associated with
brain herniation and compression of
midbrain structures
- When the serum sodium decreases to less
than 115 mEq/L, signs of increasing
intracranial pressure such as lethargy,
confusion, muscle twitching, focal
weakness, hemiparesis, papilledema,
seizures, and death.
Use AVP receptor antagonists which
stimulates free water excretion
Nursing management: I&O and daily body weight
- Athletes used to take salt tablets because
of sweating this is not recommended
- Elderly are after overlooked cause of
confusion, they are more at risk due to
renal function and subsequent inability to
excrete excess fluids. Decreased sense of
thirst.
- Patient taking lithium
Assessment and diagnostic findings:
- Primarily to sodium loss, the urinary
sodium content is less than 20 suggesting
increased proximal reabsorption of
sodium secondary to ECF volume
depletion and the specific gravity is low.
- It can also be due to SIADH, the urinary
sodium content is greater than 20 and the
urine specific gravity is usually greater
than 1012. Although the patient retains
water abnormally and therefore gains
body weight there is no peripheral edema;
instead fluid accumulates inside the cells
and this phenomenon sometimes
manifests as pitting edema
○ Hypernatremia
■ Serum sodium level higher than 145.
■ Caused by a gain of sodium in excess of water or by a loss of water in
excess sodium.
■ Can occur in patients with normal fluid volume or FVD and FVE
■ Loses more water than sodium
Pathophysiology: common cause is fluid deprivation in
patients who cannot respond to thirst such as very old
Medical management: gradual lowering of the serum
sodium level by the infusion of hypotonic electrolyte
and young and cognitively impaired patients.
- Administration of hypertonic enteral feedings
without adequate water supplements, watery
diarrhea and increased insensible water
loss(burns).
- Diabetes insipidus
- Less common causes: heart stroke, near
drowning in seawater, malfunction of
hemodialysis or peritoneal dialysis systems
- IV admin of hypertonic saline or excessive use
of sodium bicarb
solution( 0.3% sodium chloride or an isotonic non
saline solution(dextrose 5% in water aka D5W). d5w
indicates that water needs to be replaced without
sodium, it decreases the risk of cerebral edema.
- As a general rule, the serum sodium level is
reduced at a rate no faster than 0.5 - 1
mEq/L/h to allow sufficient time for
readjustment through diffusion across fluid
compartments.
- If you have diabetes insipidus desmopressin
acetate, a synthetic ADH may be prescribed.
Clinical manifestations: thirst, elevated temp, swollen
tongue and sticky mucous membranes, hallucination,
lethargy, restlessness, irritability, seizures, pulmonary
edema, hyperreflexia, twitching, nausea, vomiting,
anorexia, increased pulse and BP
Nursing management: assess for abnormal losses of
water or low water intake and for large gains of
sodium, as might occur with ingestion of OTC
medications that have a high sodium content. Thirst
and elevated body temp. Changes in behavior such as
restlessness, disorientation and lethargy
Assessment and diagnostic findings: serum sodium
level exceeds 145 and the serum osmolality excreeds
300. Urine specific gravity and urine osmolality are
increased as the kidneys attempt to conserve water.
Preventing: providing oral fluids at regular intervals,
who are unable to perceive or respond to thirst.
Parenteral or enteral tube feeding
○ Potassium imbalances (hypokalemia, hyperkalemia) K+
■ Normal serum potassium concentration is 3.5-5 mEq/L
■ 98% of body’s potassium is in the cells. The 2% is in the ECF and is
important in neuromuscular function
■ Influences both skeletal and cardiac muscle
■ To maintain balance, the renal system must function because 80% of the
potassium excreted daily leaves the body by way of the kidneys; the other
20% is lost through the bowel and in sweat
■ The kidneys regulate potassium by adjusting the amount that is excreted
in the urine.
○ Hypokalemia
■ Below 3.5 mEq/L
■ When alkalosis (high blood pH) is present a temporary shift of serum
potassium into the cells occurs
Pathophysiology: medications that lose potassium:
thiazides, loop diuretics, corticosteroids, sodium
penicillin, amphotericin B. vomiting, gastric
suctioning, diarrhea, on insulin, alcoholism or
anorexia nervosa.
- Alterations in acid- base balance due to
shifts of hydrogen and potassium ions
between the cells and the ECF.
Respiratory or metabolic alkalosis
- Hyperaldosteronism: increases renal
Medical management:
-
IV route for severe cases (2 mEq/L)
- KCl (potassium chloride)
Potassium acetate or potassium phosphate
potassium wasting; primary: adrenal
adenomas; secondary: cirrhosis, nephrotic
syndrome, heart failure, or malignant
hypertension
Clinical manifestations: severe can cause death
through cardiac or respiratory arrest. If prolonged
can lead to an inability of the kidneys to
concentrate urine, causing dilute urine(polyuria,
nocturia) and excessive thirst. Suppresses the
release of insulin resulting in glucose intolerance
- Sign and symptoms: fatigue, anorexia,
nausea and vomiting, muscle weakness,
polyuria, decreased BM, ventricular
asystole or fibrillation, paresthesias, leg
cramps, decreased BP, ileus, abdominal
distention, hypoactive reflexes,
-
Nursing management:
- Foods rich in potassium: bananas, melon,
citrus fruits, fresh and frozen vegetables,
lean meats, milk, and whole grains.
- Careful monitoring of fluid I&O is
necessary because 40 mEq of potassium
is lost for every liter of urine output
- ECG checked frequently
- Arterial blood gas values are checked for
elevated bicarb and pH levels
Assessment and diagnostic findings
ECG: flattened T waves, prominent U waves, ST
depression, prolonged PR interval
- Digitalis toxicity
- Metabolic alkalosis
Correcting hypokalemia: oral route is ideal to treat
mild to moderate hypokalemia cause oral
supplements are absorbed well.
- Oral supplements can produce small
bowel lesions therefore the patient must
be assessed for and cautioned about
abdominal distention, pain or GI
bleeding.
IV should be given only after adequate urine
output has been established. A decreased in urine
volume to less than 20 mL per hour for 2
consecutive hours is an indication to stop the
potassium infusion and notify the primary
provider.
- Never given by IV push or
intramuscularly to avoid replacing
potassium too quickly, IV potassium must
be given using an infusion pump with the
patient monitored by continuous ECG.
○ Hyperkalemia
■ Serum potassium level greater than 5 mEq/L
■ In older patients, there is an increased risk of hyperkalemia due to
decreases in renin and aldosterone as well as an increased number
of comorbid cardiac condition.
Pathophysiology: decreased renal excretion of
potassium, rapid admin, and movement of potassium
from the ICF compartment to the ECF compartment.
Medical management:
- Emergency pharmacologic therapy: administer
IV calcium gluconate, it antagonizes the
Commonly seen in patients with untreated kidney
injury, particularly those in whom potassium levels
increase as a result of infection or excessive intake of
potassium in food or medications.
- Patients with hypoaldosteronism or Addison
disease are at risk because deficient adrenal
hormones lead to sodium loss and potassium
retention.
- Medications: KCl, heparin, ACE inhibitors,
NSAIDs, beta blockers, cyclosporine,
tacrolimus, and potassium sparing diuretics
- In acidosis (low blood pH) potassium moves
out of the cells into the ECF.
- Extensive tissue trauma such as burns,
crushing injuries, or severe infections, lysis of
malignant cells after chemo.
-
action of hyperkalemia on the heart but does
not reduce the serum potassium concentration.
Monitor BP and ECG
IV admin of bicarb to alkalize the plasma
Glucose and insulin, Beta 2 agonists
Kylexate medication, liquid 30mL, cannot mix
with other liquids
Clinical manifestation: the earliest cardiac effects
occur at 6 when the narrow T waves, ST segment
depression, and s shortened QT interval
- cardiac effects occur at 8 mEq/L or greater the
PR interval becomes prolonged and is
followed by disappearance of the P waves.
Finally there is decomposition and widening
of the QRS complex.
- Signs and symptoms: muscle weakness,
tachycardia to bradycardia arrhythmias,
flaccid paralysis, paresthesias, intestinal colic,
cramps, abdominal distention, irritability, and
anxiety
Nursing management: I&O and observes signs and
symptoms of muscle weakness and dysrhythmias.
- An apical pulse should be taken
- Presence of paresthesias and GI symptoms
such as nausea and intestinal colic
- BUN, creatinine, glucose and arterial blood
gas values
- Avoid: potassium rich foods
Assessment and diagnostic findings:
Pseudohyperkalemia: improper collection or transport
of a blood sample, a traumatic venipuncture, and use of
a tight tourniquet around an exercising extremity while
drawing a blood sample, producing hemolysis of the
sample before analysis. Marked leukocytosis and
thrombocytosis; drawing blood above a site where
potassium is infusing.
○ Calcium imbalances (hypocalcemia, hypercalcemia)
■ More than 99% of the body’s calcium is located in the skeletal system
(bones and teeth).
■ Plays a mhor role in transmitting nerve impulses and helps regulate
muscle contraction and relaxation, including cardiac muscle. Is
instrumental in activating enzymes that stimulate many essential chemical
reactions in the body and it also plays a role in blood coagulation.
■ Normal total serum calcium level is 8.6 to 10.2 mg/dL
■ Absorbed from food: gastric acidity and vitamin D.
■ Excreted primarily in the feces
○ Hypocalcemia
■ Serum calcium value lower than 8.6 mg/dL.
■ Older adults and those with disabilities, who spend an increased amount of
time in bed because bed rest increases bone resorption
Pathophysiology: primary and surgical
hypoparathyroidism. Not only is hypocalcemia
associated with thyroid and parathyroid surgery,
but it can also occur after radical neck dissection
and is mostly likely in the first 24-48 hours of
surgery.
- Transient hypocalcemia can occur with
massive admin of citrated blood (massive
hemorrhage and shock, because citrate
can combine with ionized calcium and
temporarily remove it from the
circulation.
- Inflammation of the pancreas, kidney
injury, inadequate vitamin D
consumption, magnesium deficiency,
medullary thyroid carcinoma, low serum
albumin, alkalosis, alcohol abuse
- Meds: aluminium containing antacids,
aminoglycosides, caffeine, cisplatin,
corticosteroid, mithramycin, phosphates,
isoniazid, loop diuretics, and proton pump
inhibitors.
Clinical manifestation: Tetany, refers to the entire
symptom complex induced by increased neural
excitability, numbness, tingling of fingers, toes,
circumoral region. Seizures, carpopedal spasm,
hyperactive deep tendon reflexes, irritability,
bronchospasm, diarrhea, decreased BP.
- ECG: prolonged QT interval and
lengthened ST
- Labs: decreased Mg
- Chvostek sign: consists of twitching of
muscles innervated by the facial nerve
when the region that is about 2 cm
anterior to the earlobe just below the
zygomatic arch, is tapped
- Trousseau can be elicited by inflating the
BP cuff on the upper arm to about 20
mmHg above systolic pressure, within 2-5
minutes, carpal spasm will occur as
ischemia of the ulnar nerve develops
- Osteoporosis: characterized by loss of
bone mass, which causes bones to
become porous and brittle and therefore
susceptible to fracture
Assessment and diagnostic findings: when
evaluating serum calcium levels, the serum
albumin level and the arterial pH must also be
considered.
Medical management:
- Acute symptomatic hypocalcemia is life
threatening and requires prompt treatment
with IV admin of calcium salt.
- IV calcium salts: calcium gluconate,
calcium chloride.
- The IV site must be observed often for
any evidence of infiltration because of the
risk of extravasation and resultant
cellulitis or necrosis
- It can cause postural hypotension:
therefore the patient is kept in bed during
IV infusion
Nutritional therapy: Vitamin D may be instituted
to increased calcium absorption from the GI tract.
In addition, aluminum hydroxide, calcium acetate
or calcium carbonate antacids may be prescribed to
decrease elevated phosphorus levels.
Calcium containing foods: milk products, green,
leafy veggies; canned salmon, canned sardines,
and fresh oysters
Too rapid IV admin of calcium can cause cardiac arrest, preceded by bradycardia.
Therefore calcium should be diluted by d5W and given as a slow Iv bolus or a slow IV
infusion using an infusion pump.
○ Hypercalcemia
■ Serum calcium value greater than 10.2 mg/ dL
■ Mortality rate as high as 50% if not treated promptly
Pathophysiology: common causes are
malignancies and hyperparathyroidism. The
excessive PTH secretion associated with
hyperparathyroidism causes increased release of
calcium from the bones and increased intestinal
and renal absorption of calcium.
- Bone mineral is lost during
immobilization and sometimes this causes
elevation of total calcium in the blood
steam (rare)
- Thiazide diuretics, Vitamin A and D
intoxication, chronic lithium use and
theophylline toxicity.
Clinical manifestation: muscular weakness,
constipation, anorexia, nausea and vomiting,
polyuria and polydipsia, dehydration, hypoactive
deep tendon reflexes, lethargy, deep bone pain,
pathologic fractures, flank pain, calcium stones
- ECG: shorted ST segment and QT
interval, bradycardia, heart blocks
Assessment and diagnostic findings: the double
antibody PTH test, X Rays, urine calcium
Medical management: treating underlying cause
- Admin of fluids to dilute serum calcium
and promote its excretion by the kidneys,
mobilizing the patient and restricting
dietary calcium intake
- IV admin of 0.9% sodium chloride
solution temporarily dilutes the serum
calcium level and increases urinary
calcium excretion by inhibiting tubular
reabsorption of calcium
- Iv phosphate, furosemide, calcitonin,
mithramycin
○ Magnesium imbalances (hypomagnesemia, hypermagnesemia)
■ Intracellular cation. It acts as an activator for many intracellular enzyme
systems and plays a role in both carbs and protein metabolism
■ Normal level is 1.3 to 2.3 mg/dL
■ Important in neuromuscular function. It act directly on the myoneural
junctions
■ Affects the cardiovascular system, acting peripherally to produce
vasodilation and decreases peripheral resistance
○ Hypomagnesemia
■ Below 1.3 mg/ dL and is frequently associated with hypokalemia and
hypocalcemia
■ Similar to calcium in two aspects
● 1. It is the ionized fraction of magnesium that is primarily involved
in neuromuscular activity and other physiologic processes
● 2. Magnesium levels should be evaluated in combination with
albumin levels
○ 30% is protein bound, principally to albumin, a decreased
serum albumin level can reduce the measured total
magnesium concentration, however it does not reduce the
ionized plasma magnesium concentration
Pathophysiology: important route of magnesium
loss is in the GI tract; such loss can occur with
nasogastric suction(prolonged and not replaced
through IV infusion), diarrhea, or fistulas. Any
disruption in small bowel functions leads to mg
loss because the distal small bowel is the major
site of mg absorption.
- Common and overlook in acutely and
critically ill patients
- Withdrawal from alcohol and admin of
tube feedings of parenteral nutrition
- Chronic alcohol abuse should be
measured at least every 2 to 3 days
- Meds: aminoglycosides, cyclosporine,
cisplatin, diuretics, digitalis and
amphotericin, rapid admin of citrated
blood, especially patients with renal and
hepatic disease
- Diabetic ketoacidosis
Clinical manifestations: directly from the low
serum magnesium levels or due to secondary
changes in potassium and calcium metabolism
- Signs and symptoms: neuromuscular
irritability, positive Trousseau sign and
Chvostek sign, insomnia, mood changes,
anorexia, vomiting, increased tendon
reflexes, and increased BP
- ECG: PVCs, flat or inverted T waves,
depressed ST segment, prolonged PR
interval, and widened QRS
- Marked alterations in psychological
status: apathy, depressed mood,
apprehension, and extreme agitation,
ataxia, dizziness, insomnia, confusion,
delirium, auditory or visual hallucination
and frank psychoses
- Increased susceptibility to digitalis
toxicity
Assessment and diagnostic findings: serum
magnesium level is less than 1.3 mg/dL.
Medical management:
- Mild cases: can be corrected by diet
alone.
- Green leafy veggies, nuts, seeds,
legumes, whole grains, seafood,
peanut butter, and cocoa
- Magnesium salts can be given
orally in an oxide or gluconate
form to replace continuous
losses but can produce diarrhea
- IV magnesium sulfate must be
given by an infusion pump and
at a rate not to exceed 150
mg/min or 67 mEq over 8 hours
Nursing management: patient receiving digitalis
are monitored closely because a deficit of mg can
predispose them to digitalis toxicity. If they are
severe, seizure precautions are implemented
Patients should be screened for dysphagia
○ Hypermagnesemia
■ Serum magnesium level higher than 3.0 mg/dL is a rare electrolyte
abnormality, because the kidneys efficiently excrete magnesium
■ Can appear falsely elevated if blood specimens are allowed to hemolyze or
are drawn from an extremity with a tourniquet that was applied too tightly
Pathophysiology: most common cause is kidney
injury.
- Untreated diabetic ketoacidosis when
catabolism causes the release of cellular
magnesium that cannot be excreted
because of profound fluid volume
depletion and resulting oliguria.
- Excessive magnesium: given to treat
hypertension of pregnancy or to treat
hypomagnesemia
- Adrenocortical insufficiency, addison
disease, hypothermia
- Meds: antacids or laxatives, meds that
decrease GI motility(opioids and
anticholinergics)
- Lithium intoxication, extensive soft tissue
injury or necrosis as with trauma
Clinical manifestations: acute elevation of
magnesium depresses the CNS and the peripheral
neuromuscular junction.
- Coma, atrioventricular heart block,
cardiac arrest, platelet clumping, delayed
thrombin formations
- Signs and symptoms: flushing,
hypotension, muscle weakness,
drowsiness, hypoactive reflexes,
depressed respirations, cardiac arrest,
coma, diaphoresis
- ECG: tachycardia to bradycardia,
prolonged PR interval and QRS, peaked T
waves
Assessment and diagnostic findings: serum
magnesium level is greater than 3.0 mg/ dL
- Increased potassium and calcium are
present concurrently
- As creatinine clearance decreases to less
than 3.0 mL/min the mg levels increase
Medical management: can be prevented by
avoiding the admin of magnesium to patients with
kidney injury and by carefully monitoring
seriously ill patients who are receiving magnesium
salts
- Severe: all parenteral and oral magnesium
salts are discontinued.
- Emergency: respiratory depression or
defective cardiac conduction, ventilatory
support and IV calcium gluconate are
indicated
- Hemodialysis with magnesium free
dialysate, loop diuretics sodium chloride
or lactated ringer IV solution, IV calcium
gluconate
Nursing management: nurse monitors VS, noting
hypotension and shallow respirations.
- Decreased deep tendon reflexes and
changes in level of consciousness
➢ Acid base disturbances
○ Critical care units
○ Plasma pH is an indicator of hydrogen ion concentration and measures the
acidity or alkalinity of the blood.
■ Homeostatic mechanisms keep pH within normal range which is
7.35 to 7.45
● Consist of: buffer systems, kidneys, and the lungs
■ The greater the hydrogen concentration the more acidic the
solution and the lower the pH. The lower the hydrogen
concentration the more alkaline the solution and the high the pH.
○ The body's major extracellular buffer system is the bicarbonate- carbonic
acid buffer system, which is assessed when arterial blood gases are
measured.
○ The kidneys regulate the bicarb level in the ECF; they can regenerate
bicarb ions as well as reabsorb them from the renal tubular cells.
■ In respiratory acidosis and most cases of metabolic acidosis, the
kidneys excrete hydrogen ions and conserve bicarb ions to restore
balance.
■ In respiratory and metabolic alkalosis, the kidneys retain hydrogen
ions an excrete the bicarb ions to help restore balance.
○ The lungs, under the control of the medulla, control the CO2 and thus the
carbonic acid content of the ECF. thye do so by adjusting ventilation in
response to the amount of CO2 in the blood.
■ In metabolic acidosis, the RR increases, causing greater
elimination of CO2
■ In metabolic alkalosis, the RR decreases, causing CO2 to be
retained
➢ Parenteral fluid therapy
○ Goals
■ To provide water, electrolytes, and nutrients to meet daily requirements
■ To replace water and correct electrolyte deficits
■ To administer medications and blood products
➢ Systemic IV complications
○ Fluid overload: increased BP and CVP
■ Signs and symptoms: moist crackles on auscultation of the lungs, cough,
restlessness, distended neck veins, edema, weight gain, dyspnea, and
rapid, shallow respirations.
■ Possible causes: rapid infusion of IV or hepatic, cardiac or renal disease.
■ Treatment: decreasing IV rate, monitoring VS frequently, assessing breath
sounds, placing the patient in a high Fowler’s position.
■ Can be avoided: using an infusion pump
■ Complications: heart failure and pulmonary edema
○ Air embolism
■ Most often associated with cannulation of central veins and directly
related to the size of embolus and the rate of entry. Air entering into
central veins gets to the right ventricle, where it lodges against the
pulmonary valve and blocks the flow of blood from the ventricle into the
pulmonary arteries.
■ Clinical manifestations: palpitations, dyspnea, continued coughing, jugular
venous distention, wheezing, and cyanosis, hypotension; weak, rapid
pulse; altered mental status; chest, shoulder and low back pain
■ Treatment: clamping the cannula and replacing a leaking or open infusion
system; place the patient on the left side in the Trendelenburg position,
assessing VS and breath sounds, administer oxygen.
■ Complications: shock and death
○ Infection
■ Signs and symptoms: abrupt temperature elevation shortly after the
infusion is started, backache, headache, increased pulse and RR, nausea
and vomiting, diarrhea, chills and shaking, general malaise
● Additional: erythema, edema, and induration or drainage at the
insertion site
● Severe sepsis: vascular collapse, septic shock
➢ Managing local complications
○ Infiltration and extravasation
■ Infiltration: the unintentional admin of a non vesicant solution or med into
the surrounding tissue. This can occur when the IV cannula dislodges or
perforates the wall of the vein
● Characterized by: edema around the insertion site, leakage of IV
fluid from the insertion site, discomfort and coolness in the area of
infiltration, and a significant decrease in the flow rate
● Nurse: stop the infusion, sterile dressing applied to the site
● Should be started in a new site
■ Extravasation: an inadvertent admin of vesicant or irritant solution or med
into the surrounding tissue.
● Meds such as vasopressors, potassium and calcium preparation and
chemotherapeutic agents can cause pain burning and redness at the
site. Blistering, inflammation and necrosis of tissues can occur
● Nurse: stop and notify the provider
○ Phlebitis
■ Inflammation of a vein.
■ Chemical: caused by an irritating med or solution, rapid infusion rates and
med incompatibilities
■ Mechanical: long periods of cannulation, catheters be flexed areas catheter
gauges larger than the vein lumen, and poorly secured catheters
■ Bacterial: can develop from poor hand hygiene, lack of aseptic technique
failure to check all equipment before use
■ Treatment: discontinue the IV line and restarting it in another site and
applying a warm, moist compress to the affected site
○ Thrombophlebitis
■ To the presence of a clot plus inflammation in the vein. It is evidenced by
localized pain, redness, warmth and swelling around the insertion site or
along the path of the vein, immobility of the extremity because of
discomfort and swelling, sluggish flow rate, fever, malaise, and
leukocytosis
■ Treatment: discontinue the IV infusion, applying a cold compress first to
decrease the flow of blood and increase platelet aggregation, followed by a
warm compress; elevating the extremity and restarting the line in the
opposite extremity.
○ Hematoma
■ Results when blood leaks into tissues surounding the IV insertion site
■ Can result if the opposite vein wall is perforated during venipuncture, the
needle slips out of the vein, a cannula is too large for the vessel, or
insufficient pressure is applied to the site after removal of the needle or
cannula
■ Signs: ecchymosis, immediate swelling at the site, and leakage of blood at
the insertion site
■ Treatment: removing the needle or cannula and applying light pressure
with a sterile, dry dressing; applying ice for 24 hours to the site to avoid
extension of hematoma; elevating the extremity to meximize venous
return, if tolerated; assessing the extremity for any circulatory, neurologic,
or motor dysfunction; and restarting the line in the other extremity if
indicated
○ Clotting and obstruction
■ Result of kinked IV tubing, a very slow infusion rate, an empty IV valve
or failure to flush the IV line after intermittent med or solution admin
■ Signs: decreased flow rate and blood backflow into the IV tubing