Bulauitan Altered Fluid, Electrolyte 1 of 26

and Acid-Base Balance

ELECTROLYTE IMBALANCES - Renal disease (scarred distal convoluted

tubule)
‣ Inadequate Sodium Intake
Sodium Imbalances: Sodium is the - NPO
most abundant electrolyte in the ECF. - Low-Salt Diet
• Normal Range: 135-145 mmol/L ‣ Relative Sodium Deficits/Dilution of
• Functions: Serum Sodium
- Regulates the fluid volume of ECF - Excessive ingestion of hypotonic
- Maintain plasma volumes and solution
regulates size of the vascular space - Psychogenic polydipsia
- Controls body H2O distribution by - Freshwater drowning
maintaining the osmotic equilibrium - Renal failure (nephrotic syndrome)
between ICF and ECF. - Irrigation with hypotonic fluids
- Aid in conduction of nerve impulses - Syndrome of inappropriate antidiuretic
- Control muscle contractility hormone secretion (SIADH)
especially cardiac muscle - Hyperglycemia
- Maintenance of neuromuscular - Congestive heart failure
irritability and acid-base balance
• A loss or gain of sodium is usually Clinical Manifestations
accompanied by a loss or gain of water

‣ Hyponatremia: loss of total body sodium,

Sodium Deficit (Hyponatremia) the movement of sodium from the blood to
other fluid spaces, or the dilution of serum
from excessive water in the plasma
‣ Serum sodium level: <135mEq/L ‣ The Manifestations of hyponatremia are
(135mmol/L). caused by its effects on excitable cellular
activity. The cells especially affected are
‣ Pathophysiology: those involved in cerebral, neuromuscular,
- Hyponatremia primarily occurs due to and gastric smooth muscles
an imbalance of water rather than
sodium because sodium is the major a. Cerebral Manifestations:
cation in the blood and interstitial fluid Changes in cerebral function are the
and maintains the osmolarity of these most obvious problems of hyponatremia,
fluids these changes may be seen as either
depressed activity or excessive activity
‣ Two Mechanisms involved that can cause (and sometimes both).
problems of Hyponatremia are: - Behavioral or Personality changes
1. Change in excitability: sodium level in resulting from cerebral edema and
the blood and other ECF decreases, increased intracranial pressure such as
the difference in sodium levels irritability and agitation.
between the ECF and the cellular - Headache>Coma>Death
fluid also decreases. ✓ Closely observe and document client’s
2. Movement of water from ECF space behavior and level of consciousness
into the cells resulting to swelling and
impaired functions b. Neuromuscular Manifestations:
Assess the client’s neuromuscular status
Common Causes for any changes from baseline>
- Generalized skeletal muscle weakness
occurs bilaterally and is worse in the
‣ Due to Actual Sodium Deficit or legs and arms.
Increased Sodium Excretion - Diminished muscle tone and deep
- Excessive diaphoresis tendon reflexes
- Diuretics (high-ceiling diuretics)
- Wound drainage (especially
gastrointestinal)
- Decreased section of aldosterone
- Hyperlipidemia
Bulauitan Altered Fluid, Electrolyte 2 of 26
and Acid-Base Balance

c. Gastrointestinal Manifestations: f. Renal Manifestations

The smooth muscle of the GI system - Increased urine output
response to decreased serum sodium - Decreased urine specific gravity
levels with increased motility causing
- Nausea g. Integumentary Manifestations
- Diarrhea - Dry skin
- Abdominal cramping - Pale, dry mucous membrane
- Hyperactive bowel sounds, listen to
bowel sounds (with rushes and gurgles Signs of increasing intracranial pressure
over the splenic flexure and the lower such as:
left quadrant) • Lethargy
- Bowel movements are frequent and • Confusion
watery • Muscle twitching
- Peristaltic movements may be palpated • Focal weakness
and may be visible on the abdominal • Hemiparesis
surface • Pailledema
• Seizure>Death may occur
d. Cardiovascular Manifestations:
Hyponatremia has little effect on cardiac Medical Management:
muscle contractility but cardiac output is
changed with hyponatremia
‣ In Mild Hyponatremia:
- When hyponatremia occurs with
- Restrict fluid intake
changes in blood volumes, these fluid
- Oral Na supplements
changes alter cardiac function
‣ Hyponatremia r/t Hypovolemia
- In Normal Clients:
- Isotonic fluid such as NS or LR to
• Rapid Pulse rate
restore both sodium and fluid volume
• Normal BP
- High Na Foods
- In Hypovolemic (decreased plasma
‣ For severe Hyponatremia:
volume or fluid deficit) clients
- Hypertonic saline solution such as 3%
• Rapid pulse rate
or 5% NaCl infusion causes water to
• Pulse quality thready and weak
shift out of cells may lead to
• Decreased diastolic pressure
intravascular overload and brain
• Severe hypotension when moving
damage - must be given in small-
from lying to sitting position to a
volume. Monitor infusion rate and
standing position
client’s response
• Central venous pressure normal or
- Furosemide: slow infusion usually
low
administered simultaneously with
• Flat neck veins in supine position
hypertonic saline may prevent fluid
- In Hypervolemic (increased plasma
volume overload
volume or fluid excess) clients
- Monitor for neurologic and/or
• Cardiac changes include a full-
neuromuscular manifestations of
pulse, rapid, bounding pulse with
hyponatremia (lethargy, increased ICP,
normal or high bp
confusion, headache, seizures, coma,
• Central venous pressure is normal
fatigue, tremors, apprehension, muscle
or high depending on how well the
weakness, and hyerreflexia
left ventricle handles the extra fluid.
- Monitor for cardiovascular
manifestations of hyponatremia
e. Respiratory Manifestations:
(elevated BP, cold and clammy skin,
Late manifestations related to skeletal
and hypovolemia)
muscle weakness:
- For patient taking lithium: the nurse
- Shallow, ineffective respiratory
observes for lithium toxicity, particularly
movements
when sodium is lost by abnormal route
- Hypervolemia
- Supplemental salt and fluid are
- Pulmonary edema
administered: For all patients on
- Rapid, shallow respirations
lithium- adequate salt intake should be
- Moist Crackles
ensured
Bulauitan Altered Fluid, Electrolyte 3 of 26
and Acid-Base Balance

Laboratory and Diagnostic Findings: Clinical Manifestations:

‣ Na levels less than 135mEq/L regardless of ‣ The manifestations of hypernatremia

the cause of hyponatremia. involve changes in excitable membrane
- In SIADH: may lower than 100mEq/L activity, especially cerebral, neuromuscular,
‣ Urine specific gravity is low (1.002 to and cardiac functions
1.004). ‣ Thirst: is the primary characteristic of
- Hyponatremia due to SIADH, urine hypernatremia. It is a strong defender of
specific gravity is less than 1.012 serum sodium level

a. Central Nervous System

Manifestations:
Sodium Excess (Hypernatremia)
altered cerebral function is most common
problem of hypernatremia
✓ Assess the client’s mental status
‣ Serum sodium level >145mEq/L. - In hypernatremia with normal or
‣ It can be caused by a gain of sodium in decreased fluid volume:
excess of water or by a loss of water in - the client may have short attention
excess of sodium span and may be agitated or
‣ In sodium excess, the patient ingests or confused about recent events.
retains more sodium than water. Seizures may occur if serum sodium
continues to rise.
‣ Pathophysiology: - When hypernatremia occurs with blood
As serum sodium levels rises → Increases volume overload, the client may be
sodium lvls btw ECF & ICF → Increases in lethargic, drowsy, stuporous and even
osmolarity lvls of the ECF → the problem comatose
causes water to move from the cells into
the ECF to dilute the hyperosmoloar ECF b. Neuromuscular Manifestations:
→ as hypernatremia persists or worsens, Skeletal muscles responses vary with
compensatory actions cause → Severe degree of sodium increase
cellular dehydration - In Mild or Early hypernatremia:
- Spontaneous muscle twitching
Common Causes of Hypernatremia - Irregular muscle contraction
- In Severe Hypernatremia:
- Skeletal muscle weakness, the
‣ In Actual Sodium Excesses or
muscles become progressively
Decreased Sodium Excretion:
weaker with rigid paralysis
- Hyperaldosteronism
- Diminished or absent deep tendon
- Renal failure
reflexes
- Corticosteroids
- Cushing syndrome or disease ✓Assess neuromuscular status by
observing for twitching in muscle
group.
‣ In Relative Sodium Excess Decreased
Water Intake
c. Cardiovascular Manifestations
- NPO
- Decreased cardiac contractility
- Diminished cardiac output
‣ In increased Water Loss
- HR and BP respond to vascular volume
- Increased rate of metabolism
- Asses cardiac status by measuring bp
- Fever
and the rate and quality of the apical
- Hyperventilation
and peripheral pulses.
- Infection
- PR and BP may be normal, above
- Excessive diaphoresis
normal or below normal depending on
- Watery diarrhea
the fluid volume and how rapidly the
- Dehydration
imbalance occurred.
Bulauitan Altered Fluid, Electrolyte 4 of 26
and Acid-Base Balance

- In Hypernatremia with Hypovolemia: Medical Management

- PR is increased and peripheral
pulses are difficult to palpate and
Treatment of hypernatremia consists of
are easily blocked.
gradual lowering of serum sodium level
- Hypotension and severe orthostatic
‣ Other interventions used when sodium
(postural) hypotension are present
level become life-threatening include:
and pulse pressure is reduced
Hemodialysis and blood ultrafiltration
- In Hypernatremia with Hypervolemia:
- Slow to normal bounding pulses
Drug Therapy
- Peripheral pulses are full and
difficult to block
- Distended neck veins even in ‣ Hypotonic IV infusions, usually 0.25% or
upright position. 0.45% NaCl are prescribed.
- Increased diastolic blood pressure ‣ Isotonic NaCl solutions
‣ Diuretics such as furosemide (Lasix,
d. Respiratory Manifestations: Furoside), bumetanide (Bumex), and
problems associated with pulmonary ethacrynic acid (Edecrine)
edema when hypernatremia is ‣ Desmopressin acetate (DDAVP) - a
accompanied by hypervolemia synthetic antidiuretic hormone, may be
prescribed to treat diabetes insipidus if it is
e. Renal Manifestations the cause of hypernatremia
‣ Decreased urine output ‣ Assess the client hourly for symptoms of
‣ Increased urine specific gravity excessive fluid, sodium or potassium

f. Integumentary Manifestations Diet Therapy

‣ Dry, flaky skin
‣ Presence or absence of edema r/t
‣ Dietary sodium restriction may be needed
accompanying fluid volume changes
to prevent sodium excess when renal
problems are present
Laboratory and Diagnostic Findings
‣ Collaborate with the dietitian to teach the
client how to determine the sodium
‣ Increased serum sodium level exceeds 145 content of foods, beverages, and drugs
mEq/L and serum osmolality exceeds 300 ‣ Stress the importance of adhering to the
mOsm/kg diet
‣ Increased urine specific gravity and urine ‣ Fluid restriction must be followed
osmolality
‣ Patients with nephrogenic or central Nursing Management
diabetes insipidus have hypernatremia and
produce a dilute urine with urine osmolality
‣ Electrolyte Management: Hypernatremia
less than 250 mOsm/KG
- Monitor for indications of dehydration
(eg, decreased sweating, decreased
Common Nursing Diagnoses and
urine, decreased skin turgor, and dry
Collaborative Problems
mucous membrane).
- Monitor vital signs as appropriate
‣ Excess fluid volume r/t excess sodium - Weigh client daily and monitor trends
intake - Promote comfort measures to decrease
‣ Decreased cardiac output r/t poo cardiac thirst
contractility - Maintain patent IV access.
‣ Risk for falls r/t skeletal muscle weakness - Monitor intake and output.
‣ Impaired memory r/t fluid and electrolyte - Provide frequent oral hygiene
imbalance - Administer isotonic (0.9%) saline,
‣ Readiness for Enhanced Nutrition r/t the hypotonic (0.45%) saline, hypotonic
need for dietary sodium restrictions (5%) dextrose, or diuretics, as
‣ Potential for Pulmonary Edema appropriate, based on fluid status and
urine osmolality.
- Maintain sodium restrictions
Bulauitan Altered Fluid, Electrolyte 5 of 26
and Acid-Base Balance

Potassium Imbalances: Common Causes of Hypokalemia

Potassium is the major intracellular
electrolyte; 98% of the body’s potassium is
inside the cells. The remaining 2% is in the ‣ In Actual Potassium Deficits:
ECF and is important in neuromuscular - Inappropriate or excessive use of
function. drugs, such as:
• Potassium influences both skeletal and • Diuretics
cardiac muscle activity. • Digitalis
• Normal Range: 3.5-5.0 mEq/L • Corticosteroids
• Normal ICF: 140 mEq/L - Increased secretion of aldosterone
• Potassium control also occurs through - Cushing’s syndrome
the kidney function because about 80% - Diarrhea
of potassium removed from the body - Vomiting
occurs via the kidney - Wound drainage (especially
• Aldosterone is the only hormone gastrointestinal)
excretion of potassium - Prolonged nasogastric suction
- Heat-induced excessive diaphoresis
- Renal disease impairing reabsorption of
Hypokalemia potassium
- NPO
‣ Is a serum potassium level <3.5 mEq/L
‣ A common electrolyte imbalance can be ‣ In Relative Potassium Deficits
life-threatening because every system is - Alkalosis
affected - Hyperinsulinism
‣ The severity of problems caused by - Hyperalimentation
hypokalemia is related to how rapidly the - Total parenteral nutrition
serum potassium level drops - Water intoxication
- IV therapy with potassium-poor solution
Pathophysiology
Clinical Manifestations

‣ Low serum potassium levels increases the

difference in the amount of potassium Severe hypokalemia can cause death
between the fluid inside the cells (ICF) and through cardiac or respiratory arrest.
the fluid outside the cells (ECF) → the cell
membrane of all excitable tissues such as a. Gastrointestinal S/S:
nerve and muscle are less responsive to Anorexia, nausea, vomiting diarrhea,
normal stimuli → When the loss of ECF ileus, distention, decrease bowel motility
potassium is gradual →Cells adjust and
cellular potassium decreases →in b. Musculoskeletal S/S:
proportion to the ECF potassium level. Muscle weakness, paralysis, leg cramps,
muscle flabbiness, paresthesias,
‣ Potassium difference btw the 2 fluid decreased muscle strength and tendon
spaces→ remained unchanged symptoms reflexes
of hypokalemia may not appear until
potassium loss is extreme c. Cardiovascular S/S:
Dysrhythmias, vertigo, postural
‣ Rapid reduction of serum potassium hypotension, flattened T wave or
levels→causes dramatic changes in inverted T waves, depressed ST
function segments prominent U wave, slow weak
pulse
‣ Hypokalemia may result either from an
actual total body potassium loss or from d. Respiratory S/S:
movement of potassium from the ECF to Shallow respirations, shortness of breath
the ICF causing a relative decrease in ECF
potassium level e. Neurologic S/S:
Fatigue, lethargy, confusion, depression
Bulauitan Altered Fluid, Electrolyte 6 of 26
and Acid-Base Balance

f. Renal S/S: and the rate not faster than 10-20 mEq/
Polyuria, nocturia, decreased serum l concentration greater than 20 mEq/
osmolality 100 should be administered thru a
central IV catheter
Laboratory and Diagnostic Findings: ✓ Mix IV solution when adding KCl as
incorporation.
✓ NPO and post-op clients should be on
‣ ECG changes, such as:
maintenance dose at 20-40mEq/L in
- Depressed ST segment
the IV
- Flattened or inverted T wave
✓ Renal function should be monitored
- Prominent U wave- seen in extreme
thru BUN and creatinine levels and
hypokalemia
urine output
‣ Decreased K level
‣ Elevated pH and bicarbonate level
Common Nursing Diagnoses and
‣ Decrease serum Mg level
Collaborative Problems
‣ Increased 24H urine level

‣ Impaired Physical Mobility r/t skeletal

weakness
‣ Decreased Cardiac Output r/t dysrhythmias
‣ Risk of Fall r/t skeletal muscle weakness
‣ Constipation r/t smooth muscle atony
‣ Potential for Respiratory Insufficiency

Nursing Interventions

‣ The priorities for nursing care of patient

with hypokalemia are: ensuring adequate
oxygenation, patient safety for alls
prevention, and prevention of injury from
potassium administration and monitoring
the patient’s response to therapy
Medical Management: ‣ Drug and nutrition therapies help restore
normal serum potassium levels
‣ Monitor patients who are at risk -
‣ If hypokalemia cannot be prevented by implement safety measures to clients with
conventional measures such as increased
muscle weakness from hypokalemia.
intake in the daily diet or by oral potassium
‣ Eliminating hazards and assisting with
supplements for deficiencies, then it is
ambulation
treated cautiously with IV replacement
‣ Encouraging the patient at risk to eat foods
therapy
rich in potassium.
‣ Monitor heart rate and rhythm
‣ Oral potassium chloride (available in the
‣ Assess RR, depth and pattern
tablet and liquid form)
‣ Check O2 saturation by pulse oximetry
‣ Potassium chloride, potassium acetate,
‣ Assess respiratory muscle effectiveness by
potassium phosphate given as parenteral
checking patient’s ability to cough
or IV route
‣ Examine face, oral mucosa and nail beds
for pallor or cyanosis
➡ KCL should NEVER be given IM or given
‣ Evaluate arterial blood gas values for
as a bolus IV push and undiluted
decreased blood oxygen levels
✓ If given IV, it should be diluted a (hypoxemia) and increased arterial carbon
concentration of less than 80 mEq/L as
dioxide levels (hypercapnia)
recommended
‣ Administer prescribed supplemental
✓10 mEq/L diluted in 50-100ml potassium (PO, NG, or IV) as prescribed.
administered within 30 min - 1hr
‣ Prevent/reduce irritation from potassium
✓ Maximum concentration of potassium supplement.
that should be administered thru a
peripheral IV line is 20 mEq/1000ml
Bulauitan Altered Fluid, Electrolyte 7 of 26
and Acid-Base Balance

‣ MIO - because 40mEq of K is lost per 1L of heparin, ACE (angiotensin-converting

urine output enzyme) inhibitors, captoril, NSAIDs,
‣ Diuresis put the patients at risk for serious potassium sparing diuretics
K loss - but for patients with hypokalemia - Salt substitutes
who needs diuretics, a potassium sparing - Rapid infusion of K+ containing IV
diuretics such as spironolactone solutions
(Aldactone), triumterene (Dyrenium) and - Bolus of IV K+ injections
amiloride (Midamor) - they increase urine - Transfusion of whole blood or packed
output without increasing potassium loss. cells
‣ Monitor serum K level - Adrenal insufficiency (Addison’s
‣ Monitor for signs of hypokalemia-related disease, adrenalectomy)
metabolic alkalosis. - Renal failure
‣ Provide teaching
‣ Stop drugs that cause hypokalemia (eg ‣ Relative Potassium Excesses:
diuretics, laxative) - Tissue damage such as in burns,
crushing injuries or severe trauma -
causes an elevated ECF potassium
levels
Hyperkalemia
- Acidosis: potassium moves out of the
cells and into the ECF
‣ It is serum potassium level higher than 5.0 - Hyperuricemia
mEq/L - Uncontrolled diabetes mellitus
‣ The normal ranges for serum potassium
value is narrow but a slight increase above Clinical Manifestations:
normal values can affect excitable tissues,
especially the heart —> cardiac arrest
‣ Ask about chronic illnesses particularly
renal disease and diabetes mellitus, recent
Pathophysiology
medical or surgical treatment, and urine
output, including frequency and amount of
‣ A high serum potassium level decreases voiding.
the potassium difference between the ICF ‣ Ask about drug use, particularly potassium-
and the ECF → this decreased difference sparing diuretics and ACE inhibitors
increases cell excitability, as a result ‣ Diet history: intake of potassium-rich foods
excitable tissues respond to less intense and use of salt substitutes
stimuli → altered cardiac function→
sudden rises in serum potassium levels a) Cardiovascular changes:
between 6-7 mEq/L → Severe problems such as Bradycardia, hypotension and
ECG changes: Tall, peaked T waves,
‣ Hyperkalemia may result from an actual prolonged PR intervals, flat or absent P
increase in total body potassium or from waves and wide QRS complexes
the movement of potassium from the cells - As serum potassium rises -> hearbeat
to the blood generated outide the normal
conduction system in the ventricle
3 Major Causes for Hyperkalemia (ectopic beats) may appear ->
complete heart block, asystole and
ventricular fibrillation may occur, a life-
1. Decreased renal excretion of
threatening complication of severe
potassium
hyperkalemia.
2. Rapid administration of potassium
3. Movement of potassium from the ICF
b) Neuromuscular Changes:
compartment to the ECF compartment
such as skeletal muscle twitching; tingling
and burning sensations followed by
Common Causes of Hyperkalemia:
numbness in the hands and feet and
around the mouth (paresthesia) - early
‣ Actual Potassium Excesses stages of hyperkalemia
- Over ingestion of foods or medicines - As hyperkalemia worsens -> muscle
containing K-potassium chloride, twitching changes to weakness
Bulauitan Altered Fluid, Electrolyte 8 of 26
and Acid-Base Balance

followed by flaccid paralysis. the antagonistic effect of K+ excess in the

weakness moves up from the hands mycardium
and feet and affects the muscles of the - Kayexelate (polysterane sulfonate) may
arms and legs be given orally or rectally.
- Peritoneal Dialysis or Hemodialysis
c) Intestinal Changes:
such as Increased motility: causing Nursing Interventions:
diarrhea and spastic colonic activity

‣ Interventions for hyperkalemia are aimed at

Diagnostic Findings:
rapidly reducing the serum potassium
level, preventing recurrences and ensuring
‣ Potassium level over 5.0 mEq/L patient safety during the electrolyte
‣ Levels of other electrolytes, hematocrit and imbalance
hemoglobin are elevated. - IV infusion of insulin and glucose or
‣ Elevated serum creatinine, and BUN, NaHCO3 to promote K+ uptake into
decreased blood pH and normal or low the cells.
hematocrit and hemoglobin levels - Observe patient manifestations of
‣ ECG changes: Tall, peaked T waves, hypokalemia and hypoglycemia during
prolonged PR intervals, flat or absent P this therapy
waves and wide QRS complexes - Loop diuretics such as furosemide
‣ Arterial blood gas analysis - may reveal - Beta-2 agonist, such as albuterol
both a metabolic and respiratory acidosis (respiratory problems)

‣ The PRIORITIES of Nursing care of patient

with hyperkalemia:
a) Close monitoring to prevent cardiac
complications
b) Assess vital signs, monitor
cardiovascular status.
c) Anticipate cardiac monitoring and a 12
lead ECG
d) Patient safety for falls prevention:
Implement safety measures, such as
• Monitoring the patient’s response
to therapy
• Monitor serum potassium levels
• Assess motor and sensory function
• Monitor neurologic status
e) Be prepared to give Calcium
Medical Management: gluconate by slow IV infusion in acute
cases of hyperkalemia
‣ Drug Therapy is main medical intervention f) Prepare the patient for the possibility
‣ Potassium level between 5.0-5.5 mEq/L: of dialysis
restriction of dietary K intake g) Great care should be taken to
‣ If potassium excess is due to metabolic administer and monitor potassium
acidosis: correcting the acidosis with solutions closely.
NaHCO3 which promotes K+ uptake into h) Provide Health Teachings:
the cells • Diet: avoid foods high in potassium
‣ Improving the urine output usually and use of salt substitutes
decreases the elevated serum K+ level. • Drugs: Administer insulin and
Potassium-wasting diuretics (furosemide) glucose and sodium bicarbonate as
can be used. or ordered)
• Recognition of the manifestation of
‣ In Severe Hyperkalemia: hyperkalemia.
- Intravenous Ca gluconate infusion or
Ca chloride to decrease the
Bulauitan Altered Fluid, Electrolyte 9 of 26
and Acid-Base Balance

‣ For Chronic hypocalcemia: occurs slowly

Calcium Imbalances: Calcium overtime → excitable membrane
is a mineral with functions closely related to manifestations may not be severe because
those of phosphorous and magnesium the body has adjusted to the gradual
• Normal Ranges: 9.0 - 10.5 mg/dl or reduction of serum calcium levels
between 2.25 - 2.75 mmol/L
• Calcium is an ion having 2 positive Common Causes of Hypocalcemia:
charges (divalent cation) that exist in
the body in a bound form and an
ionized (unbound or free form) ‣ Actual Calcium Deficit:
• Bound Calcium is usually attached to - Inadequate oral intake of calcium
serum proteins, especially albumin - Lactose intolerance
• Ionized Calcium is present in the blood - Malabsorption syndrome, such as
and other ECF as free calcium which is Celiac sprue; Crohn’s disease
in active form and must be kept within - Inadequate intake of vitamin D
a narrow range in the ECF. - End-stage kidney disease
• More than 99% of the body’s calcium is - Renal failure
located in the skeletal system; it is a - Diarrhea
major component of bones and teeth. - Steatorrhea
• About 1% of skeletal calcium is rapidly - Wound drainage (especially
exchangeable with blood calcium and gastrointestinal)
the rest is more stable and only slowly
exchanged ‣ For Relative Calcium Deficit:
• Functions: - Hyperproteinemia
- Maintaining bone strength and - Alkalosis
density - Calcium chelators or binders
- Activating enzymes - Citrate
- Allowing skeletal and cardiac - Mithramycin
muscle contraction - Penicillamine
- Controlling nerve impulse - Sodium cellulose phosphate (Calcibind)
transmission - Aredia
- Allowing blood clotting - Acute pancreatitis
• PTH and Calcitonin: controls the serum - Hyperphosphatemia
calcium level. - Immobility
- Removal of obstruction of parathyroid

Calcium Deficit (Hypocalcemia)

Clinical Manifestations
‣ Serum level <9.0 mg/dl or 2.25 mmol/L
‣ Diet history is important to assess for the
Pathophysiology risk of hypocalcemia.

‣ Calcium is stored in the bone, with only a a) Report of frequent painful muscle
small amount of total calcium present in spasma (“charley horses”) in the calf or
the ECF → has a major effect on its foot during rest or sleep.
function
b) Other information that may indicates
‣ Low Calcium Levels→ increases sodium possible hypocalcemia:
movement across excitable membranes→ - History of recent orthopedic surgery or
allowing depolarization to occur mores bone healing
easily and at inappropriate times - Endocrine disturbances and treatment;
history of thyroid surgery, therapeutic
‣ In Acute hypocalcemia: results in the rapid irradiation of the upper chest and neck
onset of life-threatening manifestations, area, or a recent anterior neck injury.
even when the serum calcium level is not
very low.
Bulauitan Altered Fluid, Electrolyte 10 of 26
and Acid-Base Balance

c) Neuromuscular Changes: ‣ Deficient knowledge (dietary calcium) r/t

- Tetany: is the most characteristic lack of exposure
manifestations of hypocalcemia and ‣ Risk for Injury r/t bone density loss
hypomagnesemia which refers to the
entire symptoms complex induced by Laboratory and Diagnostic Findings:
increased neural excitability.
- Parathesia occurs at first with
‣ Decreased calcium levels
sensations of tingling that affects the
‣ ECG changes: prolonged ST interval and
lips, nose and ears and numbness.
prolonged QT interval
- If hypocalcemia continues or worsen->
actual muscle twitching or painful
cramps and spasms occur
Medical Management
- Assess hypocalcemia by testing for
Trousseau’s and Chvostek’s sign
‣ Acute symptomatic hypocalcemia is life-
d) Cardiovascular changes: threatening and requires prompt treatment
- Heart rate may be slower or slightly with IV administration of a calcium salt.
faster than normal with a weak, thready - Parental salts include:
pulse. • Calcium gluconate
- Severe hypocalcemia: Severe • Calcium chloride
hypotension and ECG changes of • Calcium gluceptate
prolonged ST interval and prolonged
QT interval ‣ Special Precaution: Too-rapid IV
administration of calcium can cause cardiac
e) Intestinal Changes: arrest, preceded by bradycardia. Therefore,
- Increased peristaltic activity -> calcium should be diluted in D5W and
hyperactive bowel sounds administered as slow IV bolus or a slow IV
- Painful abdominal cramping and infusion using volumetric infusion pump.
diarrhea
‣ For patients receiving digitalis-derived
f) Skeletal Changes: Most common with medications:
chronic hypocalcemia. - IV administration of calcium is
- Calcium is moved from the bone dangerous because calcium ions exert
storage sites -> a loss of bone density an effect similar to that of digitalis and
(Osteoporosis) can cause digitalis toxicity with adverse
- The bones are thinner, more brittle and cardiac effect
fragile -> breaks easily with even slight
trauma ‣ A 0.9% sodium chloride solution should
- Vertebra become more compact and not be used with calcium because they
may bend forward -> leading to an cause precipitation when calcium is added.
overall loss of height.
- Ask about changes in height and ‣ Calcium replacement can cause postural
any unexplained bone pain hypotension thus the patient is kept in bed
- Observe for spinal curvatures and any during IV infusion and blood pressure is
unusual bumps or protrusions in bone monitored.
areas that may indicate old fractures.
‣ Vitamin D may be instituted to increase
Common Nursing Diagnoses and calcium absorption from the GI tract.
Collaborative problems:
‣ Aluminum hydroxide, calcium acetate or
calcium carbonate antacids may be
‣ Acute pain r/t hypocalcemia-induced
prescribed
muscle spasms and hyperactive gastric
motility
‣ Increase dietary intake of calcium to at
‣ Decreased Cardiac Output r/t
least 1000-1500 mg/day in adult.
hypocalcemia-induced dysrhthmias or
reduced myocardial contractility
‣ Calcium-containing foods include:
Bulauitan Altered Fluid, Electrolyte 11 of 26
and Acid-Base Balance

- Milk products, Green/leafy veg,

Calcium Excess (Hypercalcemia)
Canned salmon, Sardines, Fresh oyster

‣ Hypomagnesium can also cause tetany: if ‣ Serum level >10.5 mg/dl or 2.75 mmol/L,
the tetany responds to IV calcium, then a which is dangerous imbalanced when
low magnesium level is considered as a severe. Hypercalcemic crisis has a
possible cause in chronic renal failure. mortality rate as high as 50% if not treated
promptly
Nursing Management
Pathophysiology

‣ Observe for hypocalcemia in at-risk

patients ‣ Hypercalcemia is either cause by the
‣ Seizure precautions if hypocalcemia is greater amount of serum calcium that the
severe normal calcium-controlling mechanism
‣ That status of airway is closely monitored (parathyroid gland) cannot cope or that
because laryngeal stridor can occur one control mechanism is not functioning
‣ Keeping emergency equipment at bedside properly
‣ Keep emergency cart equipped with ‣ Hypercalcemia causes excitable tissues to
emergency drugs and endotracheal tray. be less sensitive to normal stimuli, thus
‣ Padding the side rails of the bed requiring a stronger stimulus to response.
‣ The excitable tissue mostly affected by
Nutrion Therapy hypercalcemia are:
- Heart
- Muscles
‣ High-calcium diet
- Nerves
‣ Calcium supplements
- Intestinal Smooth muscles
‣ Calcium is needed by many of the
Environment Management
enzymes involved in blood clotting
‣ Hypercalcemia causes faster clotting times
‣ Is needed because the excitable and excessive clotting from hypercalcemia
membranes of the nervous system and the occurs more easily in vessels with slow
skeletal system are overstimulated in blood flow
hypocalcemia
Common Causes of Hypercalcemia:
Interventions to reduce stimulation:

‣ Actual Calcium Excesses

‣ Keeping the room quiet - Excessive oral intake of calcium
‣ Limiting visitors - Excessive oral intake of vitamin D
‣ Adjusting the lighting - Renal failure
‣ Using a soft but reassuring voice - Use of thiazide diuretics

Injury prevention strategies ‣ Relative Calcium Excesses

- Hyperparathyroidism
- Malignancy: are the most common
‣ Is needed because the patient with long-
causes of hypercalcemia
standing calcium loss may be brittle, fragile
- Hyperthyroidism
bones that fracture easily and cause little
- Immobility: causes elevation of total
pain.
calcium in the bloodstream
‣ When lifting or moving a patient with
- Use of glucocorticoids
fragile bones, use a lift sheet rather than
- Dehydration
pulling the patient.
‣ Observe for normal range of joint motion
and for unusual surface bumps or
depressions over bony areas
Bulauitan Altered Fluid, Electrolyte 12 of 26
and Acid-Base Balance

Clinical Manifestations ✓ Assess abdominal size by

measuring abdominal girth

‣ The patient with mild but rapidly occurring

d) Renal Changes:
calcium excess usually has more severe
- Excessive urination
problems than the patient whose
- Severe thirst may occur with polyuria
imbalance is severe but has developed
secondary to high calcium load
slowly

e) Chronic hypercalcemia:
a) Cardiovascular Changes:
they may develop symptoms similar to
are the most serious and life-threatening
peptic ulcer disease because
problems of hypercalcemia
hypercalcemia increases the secretion of
- Mild Hypercalcemia: at first causes
hydrochloric acid and pepsin in the
increased heart rate and blood pressure
stomach
- Severe or Prolonged calcium
- The more severe symptoms tend to
imbalance: Slowed heart rate because
appear when serum calcium level is
it depresses electrical conduction.
appx. 16mg/dL (4mmol/L) or higher
✓ Measure pulse rate and bp
✴Signs and Symptoms:
- Cyanosis and pallor: it indicates a poor
• Bone Pain
tissue blood flow
• Arrhythmias
- Examine ECG tracing for dysrhythmias,
• Cardiac Arrest
especially a shortened QT interval.
• Kidney stones
- Assess for slowed or impaired blood
• Muscle Weakness
flow: blood clotting is more likely in the
• Excessiv Urination
lower legs, the pelvic region, areas
- However, some patients become
where blood flow is blocked by internal
profoundly disturbed with serum
or external constrictions, and areas
calcium levels of only 12mg/dL
where venous obstruction occurs.
(3mmol/L).
✓ Measure and record calf
- These symptoms can be resolved once
circumference; Assess for
serum calcium levels return to normal
temperature, color and capillary
after treatment
refill to determine the blood flow to
and from the area.
f) Hypercalcemic Crisis:
refers to an acute rise in serum calcium
b) Neuromuscular Changes:
levels to 17 mg/dL (4.3 mmol/L) or higher
- Severe muscle weakness and
- Severe thirst and polyuria are often
decreased deep tendon reflexes
present.
without paresthesia
- Muscle weakness, intractable nausea,
- Severe muscle weakness and bone pain
abdominal cramps, constipation, or
may also be present
diarrhea, peptic ulcer symptoms, bone
- Patient may have an altered level of
pain, lethargy, coma, and confusions
consciousness that can range from
- This condition is very dangerous and
confusion, impaired memory, slurred
may result to cardiac arrest
speech, and lethargy to coma
- Mild psychotic behavior or problems
can occur also.
Laboratory and Diagnostic Findings:

c) Intestinal Changes:
are the first reflected as decreased ‣ Serum level >10.2 mg/dL (2.6mmol/L)
peristalsis ‣ Cardiovascular changes:
- Constipation - ECG: include dysrhythmias (eg Heart
- Anorexia, nausea, vomiting and Block) and shortening of QT intervals
abdominal pain are common and ST segments. PR interval is
- Dehydration sometimes prolonged
- Bowel sounds are hypoactive or absent ‣ Doubled-antibody PTH Test may be used
- Abdomen increase in size: because the to differentiate between primary
intestinal contents remain in the tract hyperparathyroidism and malignancy as a
instead of moving forward. cause of hypercalcemia
Bulauitan Altered Fluid, Electrolyte 13 of 26
and Acid-Base Balance

‣ Increased PTH levels: indicates primary or Nursing Management

secondary hyperparathyroidism and
suppressed in malignancy
‣ Interventions for hypercalcemia aim to
‣ X-rays may reveal bone changes if the
reduce serum calcium levels through drug
patient has hypercalcemia secondary to
therapy and dialysis
malignancy, bone cavitation and renal
‣ It is important to monitor hypercalcemia in
calculi.
at-risk patients
‣ Rehydration and cardiac monitoring are
also important
Medical Management
‣ Increasing patient mobility and increasing
fluids
‣ Therapeutic management for ‣ Hospitalized patients at risk for
hypercalcemia include: hypercalcemia should be encouraged to
- Decreasing the serum calcium level and ambulate ASAP
reversing the process causing ‣ Outpatient are instructed about the
hypercalcemia importance of frequent ambulation
‣ Treating the underlying cause is essential ‣ Oral Fluids:
- The nurse should consider patients
likes and dislikes
Pharmacologic Therapy - Fluids containing sodium should be
administered unless contraindicated bc
sodium assists with calcium excretion
‣ IV administration of 0.9% sodium chloride
- Encouraged patient to drink at least 3-4
solution
qts of fluid daily
‣ Administering IV phosphate
‣ Adequate fiber in the diet to offest the
‣ Furosemide (Lasix) often used in
tendency for constipation
conjunction with administration of saline
‣ Safety precautions are implemented as
solution
necessary, when mental symptoms are
‣ Fluids and medications that contain
present
calcium and dietary sources of calcium
- The patient and family are informed
should be stopped (D/C IV with calcium
that these mental changes are
eg. PLR)
reversible with tx.
‣ Calcitonin: can be used to lower the serum
calcium level and is particularly useful for
Drug Treatment
patients with heart disease or renal failure
who cannot tolerate large sodium loads.
- Calcitonin derived from salmon is ‣ Preventing increases in calcium, as well as
commonly used (Skin testing for allergy drugs to lower calcium levels
to salmon calcitonin is necessary before - IV solutions contain calcium are
the hormone is administered) can stopped
prevent systemic allergic rxns. - Oral drugs contain calcium or Vit. D are
- Calcitonin is administered by IM D/C
injection rather than SQ - IV normal saline (0.9% NaCl) as fluid
‣ For patients with Cancer: Treatment is volume replacement
directed at controlling the condition by, - Thiazide diuretics are d/c and replaced
surgery, chemotherapy and radiation with diuretics that enhance the
therapy excretion of calcium such as
‣ Corticosteroids may be used furosemide, (lasix, furoside)
‣ Mithramycin ‣ Calcium Chelators (calcium binders) such
‣ Inorganic phosphate salts (Phospho-Soda, as plicamycin (Mithracin) and penicillamine
Neutra-Phos) can be administered orally or (Cuprimine, Pedramine) - helps lower
by NGT serum calcium levels
‣ Dialysis: for life-threatening hypercalcemia ‣ Drugs to prevent hypercalcemia include
agents that inhibit resorption from bones
such as phosphorus calcitonin (Calcimar),
biphosphates (etidronate) and
Bulauitan Altered Fluid, Electrolyte 14 of 26
and Acid-Base Balance

prostaglandin synthesis inhibitors (aspirin,

NSAIDS).

‣ Dialysis is used when severe hypercalcemia

cause life-threatening cardiac problems
and drug therapy may not reduce serum
calcium levels fast enough to prevent
death.
- Prepare patient for a possible
hemodialysis or blood ultrafiltration
‣ Cardiac Monitoring : Assess for s/s of
digitalis toxicity such as confusion, irregular
pulse, loss of appetite, nausea and
vomiting, diarrhea, palpitations an vision
changes (blurred vision, blind spots)

‣ Other symptoms: decreased

consciousness, decreased urine output,
difficult breathing when lying down,
excessive nighttime urination and
overall swelling
‣ Identify dysrhythmias and decreased
cardiac output.
‣ Compare recent ECG tracing with the
patient’s baseline tracings
‣ Look for changes in T waves and the
QT interval and changes in rate and
rhythm

if you have made it this

far studying, good job,
half way there!
Bulauitan Altered Fluid, Electrolyte 15 of 26
and Acid-Base Balance

- The effects of hypomagnesemia are

Magnesium Imbalances: caused by increased membrane
Magnesium is a mineral that forms a cation excitability and the accompanying
when dissolved in water. It is the most serum calcium and potassium
abundant intracellular cation after potassium imbalances.
• Plasma levels of free magnesium - Excitable membranes, especially nerve
range from 1.3-2.1mg/dL, or 0.65-1.05 cell membranes may depolarize
mmol/L spontaneously.
• Adults have an average total body - Hypomagnesemia is caused by
level of 25g of magnesium, most of decreased absorption of dietary
which (60%) is stored in bones and magnesium or increased renal
cartilage magnesium excretion
• Little magnesium is present in the ECF
• Much more amount of magnesium is Common Causes of Magnesium Imbalance
present in the ICF, and it has more
functions inside the cells than in the
blood ‣ For Hypomagnesemia
• Magnesium is critical for: - Malnutrition
- Skeletal muscle contraction - Starvation
- Carbohydrate metabolism - Diarrhea
- Adenosine triphosphate (ATP) - Steatorrhea
formation - Celiac disease
- Vitamin activation - Crohn’s disease
- Cell growth - Drugs (diuretics, Aminoglycoside
• Extracellular magnesium regulates antibiotics, cisplatin, amphotericin B,
blood coagulation and skeletal muscle cyclosporine)
contractility - Citrate (blood products)
• Kidneys and the intestinal tract are - Ethanol ingestion
responsible for regulation of
magnesium but exact mechanisms are Clinical Manifestations
not known.
• When blood magnesium levels are ‣ The common clinical manifestations of
low: ingestion magnesium is rapidly hypomagnesemia are seen in the
absorbed -> kidney excretion of neuromuscular, central nervous and
magnesium stops intestinal system.
• When blood magnesium levels are
high -> little magnesium is absorbed a) Neuromuscular Changes:
from food -> kidney magnesium are caused by increased nerve impulse
excretion increases. transmission
- Decreased levels increase impulse
transmission from nerve to nerve or
Magnesium Deficit from nerve to skeletal muscle
(Hypomagnesemia) - The patient has hyperactive deep
tendon reflexes, tingling, and painful
muscle contractions
- Positive Chvostek’s and Trousseu’s signs
‣ Serum level <1.3 mEq/L - Skeletal muscle weakness
- If hypomagnesemia worsens: patient
Pathophysiology: may have tetany and seizures

‣ Most problems leading to b) Central Nervous System Changes:

hypomagnesemia are caused by decreased are caused by increased nerve impulse
magnesium intake or increased magnesium transmission. These changes may present
loss as a result hypomagnesemia reflects a as psychological depression, psychosis,
decrease in the total body magnesium and confusion
content. - Alterations in mood include: apathy,
depression, apprehension, and extreme
Bulauitan Altered Fluid, Electrolyte 16 of 26
and Acid-Base Balance

agitation, as well as ataxia, dizziness, ‣ Patients receiving parenteral nutrition

insomnia, and confusion require magnesium in the IV solution - to
- At times, delirium, auditory or visual prevent hypomagnesemia.
hallucinations and frank psychoses may ‣ IV magnesium sulphate: are given for
occur severe hypomagnesemia and must be
administered by an infusion pump
c) Intestinal changes: - IV route is used because MgSO4
are from decreased intestinal smooth causes pain and tissue damage when
muscle contraction injected IM
- Reduced motility, anorexia, nausea, ‣ A bolus dose of magnesium sulphate given
constipation, and abdominal distention too rapidly can produce alteration in
are common. cardiac conduction leading to heart block
- Paralytic ileus may occur if or asystole (cardiac standstill with no
hypomagnesemia is severe cardiac output and no ventricular
depolarization)
‣ Magnesium deficiency can disturb the
ECG by prolonging the QRS, depressing
the ST segment and predisposing the
Magnesium Excess
cardiac dysrhythmias such as premature
(Hypermagnesemia)
ventricular contractions (PVC) , supra-
ventricular tachycardia and ventricular
fibrillation ‣ Serum level >2.1 mEq/L
‣ It is a rate electrolyte abnormality because
the kidneys efficiently excrete magnesium
Laboratory and Diagnostic Findings
Pathophysiology

‣ Serum level <1.3 mg/dL (0.62 mmol/L)

‣ Urine Magnesium: may help identify the ‣ By far the most common cause of
cause of magnesium depletion, and levels hypermagnesemia is renal failure
are measured after a loading dose of ‣ When magnesium excess occurs, excitable
magnesium sulphate is administered. membranes are less excitable and need a
‣ Nuclear magnetic resonance stronger-than-normal stimulus to respond.
spectroscopy and the ion selective ‣ With severe hypermagnesemia excitable
electrode: are the two newer diagnostic membranes, may not respond to any
techniques as a sensitive and direct means stimulus
of measuring ionized serum magnesium ‣ The imbalance results from intake of
levels magnesium couple with decreased renal
excretion of magnesium
Medical Management
Common Causes of Magnesium Imbalance:

‣ Mild Magnesium deficiency can be

corrected by diet alone. ‣ For Hypermagnesemia
- Principal dietary sources of magnesium: - Increased magnesium intake
green leafy veg, nuts, seeds, legumes, - Magnesium-containing antacids and
whole grains, seafood, peanut, butter, laxatives
and cocoa. - IV magnesium replacement
‣ If necessary, magnesium salts can be - Decreased renal excretion of
administered orally in an oxide or gluconate magnesium resulting from renal
form to replace continuous losses but can insufficiency
produce diarrhea.
‣ Drugs that promote magnesium loss such Clinical Manifestations:
as high ceiling (loop) diuretics,
Aminoglycoside antibiotics, and drugs
‣ Most manifestations of hypermagnesemia
containing phosphorus are d/c
occur as a result of reduced membrane
excitability. They usually are not apparent
Bulauitan Altered Fluid, Electrolyte 17 of 26
and Acid-Base Balance

until serum magnesium levels exceed 4 Laboratory and Diagnostic Findings

mEq/L.
‣ The most common problems are seen in
‣ Serum level >3.0mg/dl (1.25 mmol/L)
cardiac, central nervous system, and
‣ Increased potassium and calcium are
neuromuscular systems. *Neuromuscular
present
first to be affected*
‣ As creatinine clearance decreases the less
than 3.0ml/L, the serum magnesium levels
a) Cardiac Changes:
increase and by carefully monitoring
such as bradycardia, peripheral
seriously ill patients who are receiving
vasodilation and hypotension- these
magnesium salts.
problems become more severe as serum
- In patients with severe
magnesium levels increase
hypermagnesemia: all parenteral and
- ECG Changes: show a prolonged PR
oral magnesium salts are d/c
interval with widened QRS complex
‣ In emergencies such as respiratory
- Bradycardia can be severe and cardiac
depression or defective cardiac
arrest is possible.
conduction: ventilatory support and IV
- Hypotension is also severe, with
calcium gluconate are indicated
diastolic pressure lower than normal
‣ Hemodialysis with magnesium-free
due to peripheral vasodilation
dialysate: can reduce the serum
- Patients with severe hypermagnesemia
magnesium to a safe level within hours.
are in grave danger of cardiac arrest.
‣ Administration of loop diuretics (Lasix) and
sodium chloride or lactated Ringer’s IV
b) Central Nervous System Changes:
solution: enhances magnesium excretion in
results from depressed nerve impulse
patients with adequate renal function
transmission
‣ IV calcium Gluconate: antagonizes the
- Patients may be drowsy or lethargic
cardiovascular and neuromuscular effects
and has difficulty in speaking
of magnesium
(Dysarthria)
- Coma may occur if the imbalance is
prolonged or severe.
Nursing Management

c) Neuromuscular Changes:
results from depressed nerve impulse ‣ If hypermagnesemia is suspected, the
transmission to the skeletal muscles nurse monitors VS, noting hypotension and
- Deep tendon reflexes are reduced or shallow respirations
even absent ‣ The nurse observes for decreased deep
- Voluntary skeletal muscle contractions tendon reflexes and change sin the level of
become progressively weaker and consciousness.
finally stop ‣ Medications that contain magnesium are
not administered to patients with renal
‣ Hypermagnesemia has no direct effect on failure or compromised renal functions and
the lungs; however, when the respiratory patients with renal failure are cautioned to
muscles are weak: respiratory insufficiency check with their health care providers
→ to respiratory failure → death before taking OTC medications
‣ Caution is essential when preparing and
d) ECG findings may include: a prolonged administering magnesium-containing fluids
PR interval, tail T waves, a widened QRS, parenterally because available parenteral
and prolonged QT interval, as well as an magnesium differs in concentration
atrioventricular block

Medical Management

‣ Hypermagnesemia can be prevented by

avoiding administration of magnesium to
patients with renal failure
Bulauitan Altered Fluid, Electrolyte 18 of 26
and Acid-Base Balance

- Changing the distribution of other

Acid-Base Imbalances: Acid- electrolytes, causing fluid and
base balance occurs through control of electrolyte imbalances
hydrogen ion (H+) production and - Changing excitable membranes,
elimination. making the heart, nerves, muscles,
and the GI tract either less or more
• Plasma pH: is an indicator of hydrogen active than normal
ion (H+) concentration - Decreasing the effectiveness of
• Keeping the pH within the normal many drugs
range involves balancing acids and
bases in body fluids
• Normal pH ranges: (controlled by
homeostatic mechanisms) Acid-Base Disorders

‣ Acids: are substances that release

Arterial Blood 7.35 - 7.45
hydrogen ions when dissolved in water
Venous Blood 7.31 - 7.41 (H2O). An acid in solution increases the
amount of free hydrogen ions in that
These Mechanisms Consists of: solution
- Buffer systems ‣ Strong acid: such as hydrochloric acid
- The kidney (HCl) separates completely in water and
- The lungs readily releases all of its hydrogen ions
‣ Weak acid: such as acetic acid
• 3 Major Homeostatic mechanisms (CH3COOH) does not completely separate
maintain acid-base balance: in water, it release only some of its
1. Buffering: by extracellular and hydrogen ions
intracellular buffers - *1st line
emergency defense (rapid) ‣ Base: is a substance that binds free
2. Lungs (Alveolar ventilation): hydrogen ions in solution. Bases are
which controls PaCO2 ( and “hydrogen acceptors” that reduce the
increases efficiency of H2CO3/ amount of free hydrogen ions in solution
NaCHO3 buffer system) ‣ Strong Bases: include sodium hydroxide
3. Renal (H+ excretion): which (NaOH) and ammonia (NH3) bind
controls plasma (HCO3) and hydrogen ion easily
conserves Na+ and excretes ‣ Weak Bases: such as aluminum hydroxide
anion of the offending acid, slow. (AlOH3) and bicarbonate (HCO3) bind
hydrogen ions less readily
• The hydrogen ion concentration is
extremely important: 1. Acid-Base Regulatory Mechanism
- The greater the concentration, the
more acidic the solution and the ‣ Buffer systems:
lower the pH. are the first line of defense and prevent
- The lower the H+ concentration, major changes in the pH of body fluids
the more alkaline the solution and by removing or releasing H+ as they can
the higher the pH act quickly to prevent excessive changes
- The pH solution may range from in hydrogen ion concentration.
1-14, with 7 being neutral. ‣ Hydrogen ions:
are buffered by both intracellular and
• Keeping the pH of the blood within extracellular buffers
normal range is important because
changes from normal interfere with
many normal physiologic functions:
- Changing the shape and reducing
the function of hormones and
enzymes
Bulauitan Altered Fluid, Electrolyte 19 of 26
and Acid-Base Balance

Site Buffer system Comment

2. Respiratory Acid-Base Control
Bicarbonate Important for
Mechanism
metabolic
acids

Hemoglobin Important for ‣ When chemicals buffers alone cannot

Blood carbon dioxid prevent changes in blood pH, the
Plasma Minor buffer respiratory system is the second line of
protein defense against changes
- Breathing controls the amount of free
Phosphate Concentration
too low hydrogen ion by controlling hte amount
carbon dioxide (CO2) in arterial blood.
Proteins Important
buffer
- The lungs, under the control of hte
ICF medulla, control the CO2 and thus hte
Phosphates Important carbonic acid content of the ECF by
buffer
adjusting ventilation in response to the
Phosphate Responsible amount of CO2 in the blood
for most of - A rise in partial pressure of CO2 in
“Titrable
acidity” arterial blood (PaCO2) is a powerful
Urine
stimulant of respiration
Ammonia Important
- The partial pressure of oxygen in
formation of
NH4 arterial blood (PaO2) also influences
respiration
- In metabolic acidosis, the respiratory
rate increase, causing greater
Bicarbonate-carbonic acid buffer system
elimination of CO2 (to reduce the acid
load)
‣ is the body’s major extracellular buffer
system which is assessed when arterial ‣ Hyperventilation → increase in rate and
blood gasses are measured. depth of breathing → decreased CO2
- Normally there are 20 parts of ‣ Hypoventilation → decrease in rate and
bicarbonate (HCO3) to one part of depth of breathing → decreased CO2
carbonic acid (H2CO3); so that if this

3. Renal Acid-Base Control Mechanisms

- The kidneys are the THIRD line of

defense against wide change in body
fluid pH.
- Renal mechanisms are stronger for
regulating acid-base balance but take
longer than chemical and respiratory
mechanisms to completely respond;
they take 24-48hrs to respond

‣ Kidney movement of bicarbonate is the

first renal control mechanisms
- Much of the bicarbonate made in other
body areas is excreted in the urine
ratio is altered, the pH will change - When blood hydrogen ion levels are
‣ Intracellular buffers include protein, organic low, the bicarbonate remains in the
and inorganic phosphates, and in red urine and is excreted
blood cells, hemoglobin - When hydrogen ion excess occurs, the
kidney tubules also can make
additional bicarbonate that will be
reabsorbed.
Bulauitan Altered Fluid, Electrolyte 20 of 26
and Acid-Base Balance

‣ Formation of Acids is the second renal gasses adequately, thus CO2 is retained
control mechanisms continually and the blood pH falls
- It occurs through the phosphate (become acidic)
buffering system inside the cells of the - To oppose the process, the kidney
kidney tubules excretes more hydrogen ions and
- Once the hydrogen ion is in the urine, it increases the reabsorption of
binds to phosphate ion forming an bicarbonate back in the blood; as a
acid, H2PO4 (Dihydrogen phosphate), result, the blood pH remains either
which is excreted in the urine. within or closer to the normal range.

‣ Formation of ammonium is the third renal ‣ When these back up mechanisms are
control mechanisms completely effective:
- Ammonia (NH3): which is formed Acid-base problems are fully
during normal protein breakdown will compensated and the pH of the blood
be converted into ammonium (NH+4) returns to normal even though the levels
- The ammonia is secreted into the urine, of oxygen and bicarbonate are abnormal.
where it can combine with hydrogen
ions to form ammonium. ‣ Sometimes the respiratory problems
- The ammonium “trap” the hydrogen causing the acid-base imbalance is so
ions and then allows them to be severe that the kidney actions can only
excreted in the urine, the result is loss partially compensate, the pH is not quite
of hydrogen ions and an increase in the normal.
blood pH. Partial compensation is helpful because
it prevents the acid-base imbalance from
➡ Compensation becoming severe or life-threatening.
‣ In the process of compensation: the
body adapts to attempt to correct
changes in blood pH
Specific Acid-Base Imbalances
‣ A pH below 6.9 or above 7.8 is always
fatal.
‣ Acid-base imbalances are the changes in
‣ The normal pH range for human ECF is
the blood hydrogen ion level or pH; these
7.35 7.45.
changes are caused by problems with the
‣ Both the kidneys and the lungs can
acid-base regulatory mechanisms of the
compensate for acid-base imbalances,
body or by exposure to dangerous
but they are not equal in their
conditions
compensatory responses
↑ CO2 Acidosis
Respiratory
‣ Respiratory Compensation: ↓ CO2 Alkalosis
occurs through the lungs, usually correct
for acid-base imbalances from metabolic ↑ HCO3 Alkalosis
Metabolic
problems ↓ HCO3 Acidosis
- To bring the pH level to normal,
breathing is triggered in response to
‣ Acidosis: reflects an imbalance in which
increased CO2 levels: both the rate and
the blood pH is below normal
depth of respiration is increased; these
‣ Alkalosis: reflects an imbalance in which
respiratory efforts cause the blood to
the blood pH is above normal.
lose CO2 with each exhalation - so ECF
level of CO2 and free hydrogen ions
gradually decrease.

‣ Renal Compensation
results when a healthy kidney works to
correct for changes in the blood pH that
occur when the respiratory system is
either overwhelmed or is not healthy.
For example: A person with COPD, the
respiratory system cannot exchange
Bulauitan Altered Fluid, Electrolyte 21 of 26
and Acid-Base Balance

1. Overproduction of hydrogen ions: can

Acidosis
occur with excessive breakdown of fatty
acids, anaerobic (lactic acidosis), and
Pathophysiology: excessive intake of acids.
‣ Excessive breakdown of fatty acids
occurs with diabetic ketoacidosis or
In acidosis, the acid-base balance of the
starvation
blood and other ECF is upset by an
excess of hydrogen ion (H+) ‣ When glucose is not available for fuel
the body breaks down fats (lipids) - the
- This problem is reflected as arterial
products of excessive fatty acids
blood pH below 7.34
breakdown are strong acids
(ketoacids), which release large
‣ Acidosis is not a disease; it is a condition
amounts of hydrogen ions
caused by a disorder or pathologic
processes ‣ Lactic acidosis occurs when cells are
forced to use glucose without adequate
‣ Actual acid excess result in acidosis by
oxygen (anaerobic metabolism), as a
either overproducing acids (and release of
result; glucose is incompletely broken
hydrogen ions) or under eliminating
down → forms lactic acid
normally produced acids (retention of
hydrogen ions) ‣ Lactic acidosis occurs whenever the
body has too little oxygen such as
‣ Relative acidosis: the amount or strength
during heavy exercise, seizure activity,
of acids does not increase, instead, the
fever and reduced oxygen intake.
amount or strength (or both) of the bases
decreases (to create a base deficit) which ‣ Excessive intake of acids floods the
body with hydrogen ions
makes the fluid relatively acidic than basic
caused by either over eliminating bases ‣ Agents that cause acidosis when
ingested in excess include:
(bicarbonate ions [HCO-3]) or under
- Alcoholic beverages
producing bases.
- Methyl alcohol
- Acetylsalicylic acid (aspirin)
‣ The main problems are related to the fact
that hydrogen ions are positively charged
2. Under-elimination of hydrogen ions:
ions, thus an increase in H+ creates
leads to acidosis when hydrogen ions are
imbalances of other positively charged
produced at the normal rate but are not
electrolytes, especially K.
removed at the same rate they produced.
‣ These electrolyte imbalances then disrupt
the functions of the nerves, cardiac muscle ‣ Most hydrogen ion loss occurs through
the lungs and the kidneys
and skeletal muscle

3.Underproduction of bicarbonate ions

‣ Early manifestations of acidosis: first
(base deficit): it leads to acidosis when
appear in the:
hydrogen ion production and removal are
- Musculoskeletal, cardiac, respiratory,
normal but too few bicarbonate ions are
and central nervous systems
present to balance the hydrogen ion.
‣ Even slight increase in blood hydrogen ion
levels reduce the activity of many ‣ Such base deficits occur when
bicarbonate ions are not produced at
hormones and enzymes leading to death.
the normal rate because bicarbonate is
- Acidosis can be caused by metabolic
made in the kidneys and in the
problems, respiratory problems, or
pancreas, thus renal failure and
combined metabolic and respiratory
impaired liver or pancreatic function
problems
can cause base-deficit acidosis

4. Over-elimination of bicarbonate ions

Metabolic Acidosis
(base-deficit): leads to acidosis when
Four processes can result in metabolic hydrogen ion production and remolval are
acidosis: normal but too many bicarbonate ions
have been lost
Bulauitan Altered Fluid, Electrolyte 22 of 26
and Acid-Base Balance

Respiratory Acidosis poor gas exchange, CO2 retention and

acidosis
‣ The upper airway can be obstructed
Results when any area of the respiratory
externally by clothing, neck edema,
function is impaired, reducing the exchange
and local lymph node enlargement
of oxygen (O2) and carbon dioxide (CO2) →
CO2 retention, because any increase in CO2
4. Reduced alveolar-capillary diffusion:
levels causes the same increase in hydrogen
causes poor gas exchange, leading to
ion levels; then CO2 retention leads to
CO2 retention and acidosis.
acidosis
‣ Disorders that reduce diffusion include:
- Unlike metabolic acidosis: respiratory
pneumonia, pneumonitis, tuberculosis,
acidosis results from only one
emphysema, acute respiratory distress
mechanism: retention of CO2 causing
syndrome, chest trauma, pulmonary
increased production of free hydrogen
emoboli, pulmonary edema and
ions
drowning.

Respiratory Acidosis: is caused by four

types of problems: Combined Metabolic and
Respiratory Acidosis
1. Respiratory depression: caused by
reduced function of the brainstem neurons
‣ Uncorrected acute respiratory acidosis
that trigger breathing movements resulting
always leads to poor oxygenation and
in a reduced rate and depth of breathing
lactic acidosis
leading to poor gas exchange and
‣ Combined acidosis is more sever than
retention of carbon dioxide.
either metabolic acidosis or respiratory
‣ Respirations can be depressed also by
acidosis alone
anesthetic dugs (especially opioids) and
- Cardiac Arrest: is an example of
poisons such as methyl alcohol,
problem leading to combined
pesticides, and botulinus toxin
metabolic and respiratory acidosis
‣ Physical depression of respiration are
damaged or destroyed by trauma or
Clinical Manifestations:
when problems in other ares of the
brain increases the ICP - causing
‣ Changes occur in the excitable membranes
edema
of neurons, skeletal muscle and gastric
‣ Problems causing cerebral edema and
smooth muscle.
respiratory depression include: brain
tumors, cerebral aneurysm, stroke, and
a) Central Nervous System Changes:
overhydration
include depression of CNS function.
Problems may range from lethargy to
2. Inadequate chest expansion: reduces
confusion especially in older patients.
gas exchange and leads to acidosis
‣ Patient may become stuporous and
‣ Chest expansion can be restricted by
unresponsive
skeletal muscle trauma or deformities,
respiratory muscle weakness, or
b) Neuromuscular Changes:
external constriction.
with acidosis include:
‣ Respiratory muscle weakness: caused
‣ Reduced muscle tone and deep tendon
by electrolyte imbalances, fatigue,
relfexes (hyporeflexia)
muscle dystrophy, muscle damage or
‣ Skeletal muscle weakness → flaccid
breakdown, reducing chest
paralysis
movements.
‣ External conditions such as body casts,
c) Cardiovascular Changes:
tight scar tissue around the chest,
are first seen with acidosis and are more
obesity and ascitis can restrict chest
severe as the conditions worens
movement and gas exchange.
‣ Early changes include: increased heart
rate and cardiac output
3. Air Obstruction: prevents air movement
‣ With worsening acidosis or with
into and out from the lungs leading to
acidosis and hypekalemia: decreased
Bulauitan Altered Fluid, Electrolyte 23 of 26
and Acid-Base Balance

heart rate, tall and peaked T waves, Another table

widened QRS complexes ABG pH PaCO2 HCO3
‣ Thready peripheral pulses
‣ Hypotension Respiratory
Acidosis ⇣ ⇡ normal

d) Respiratory Changes: Respiratory

Alklosis ⇡ ⇣ normal
may cause the acidosis and can be
caused by the acidosis
‣ Kussmal respiration: breaths are deep
Metabolic
Acidosis ⇣ normal
⇣
and rapid and not under voluntary
control (in metabolic acidosis with
Metabolic
Alkalosis ⇡ normal
⇡
respiratory compensation)
‣ Shallow and rapid respiration: if Another one…
acidosis is caused by respiratory
Disorder Initial Event Compensation
problems breathing efforts are reduced
‣ Muscle weakness makes this problem Respiratory ⇣pH, ⇡ or ⇡Renal acid
worse Acidosis normal HCO3, excretion and
⇡PaCO2 ⇡serum HCO3

e) Skin Changes: Respiratory ⇡pH, ⇣ or ⇣Renal acid

occur with metabolic and respiratory Alkalosis normal HCO3 excretion and
⇣ PaCO2 ⇣ serum
acidosis HCO3
‣ Skin and mucous membrane warm, dry
and pink caused by vasodilation due to Metabolic ⇣pH, ⇣HCO3, Hyperventilati
Acidosis ⇣ or normal on with
metabolic acidosis PaCO2 resulting
‣ Pale to cyanotic and dry skin in ⇣PaCO2
respiratory acidosis (conserves
HCO3)

Metabolic ⇡pH, ⇡HCO3, Hypoventilatio

Laboratory and Diagnostic Studies Alkalosis ⇡ or normal n with
PaCO2 resulting
⇡PaCO2
‣ Arterial blood p: 7.35 indicate acidosis
‣ Other laboratory data: ABG and blood ‣ To determine if compensation has begun:
levels of electrolytes - Compensated:
pH is normal; PaCO2 and HCO3 is
- Metabolic Acidosis: abnormal
pH is low <7.35 - Partially-compensated:
pH, PaCO2 and HCO3 are all
Bicarbonate low <21 mEq/L
abnormal
Partial pressure of normal - Uncompensated:
arterial Oxygen (PaO2) ph is abnormal; either of PaCO2 and
Partial pressure of normal or slightly HCO3 is normal
arterial Carbon dioxide decreased
(PaCO2)
‣ When respiratory acidosis persist for 24
hours or longer, kidney compensation
- Respiratory Acidosis: is reflected by increases the levels of bicarbonate.
several changes in ABG values - Chronic respiratory acidosis is indicated
pH is low <7.35 by an elevated bicarbonate level and
increased PaCO2.
Bicarbonate low Variable
- Serum potassium levels are elevated in
Partial pressure of low acute respiratory acidosis
arterial Oxygen (PaO2) - They are normal or low in chronic
Partial pressure of high respiratory acidosis when renal
arterial Carbon dioxide compensation is present
(PaCO2)
Bulauitan Altered Fluid, Electrolyte 24 of 26
and Acid-Base Balance

Common Nursing Diagnoses and ✓ Use caution when giving oxygen to

Collaborative Problems patients with COPD and CO2
retention as evidenced by a high
PaCO2 level - the only breathing
‣ Nursing diagnoses that may apply to
trigger for these patients is decreased
patients with acidosis include:
arterial oxygen level.
- Deficient fluid volume r/t dehydration
- Decreased cardiac output r/t poor
‣ Giving too much oxygen to these patient
cardiac output
decreases their respiratory drive → may
lead to respiratory arrest
Interventions
- Pulmonary hygiene: promote gas
exchange with the use of positioning
‣ Metabolic Acidosis: techniques to enhance the removal of
such as hydration and drugs or lung secretions and specific breathing
treatments to control the problems techniques to keep alveoli inflated
causing acidosis ✓ Help the patient assume an upright
✓ Rehydration and antidiarrheal drugs: position (mid- to high-Fowler’s
given if acidosis is a result of prolonged position)
diarrhea ✓ Increasing fluid intake
✓ Bicarbonate is administered only if ✓ Ventilation support: with
serum bicarbonate levels are low mechanical ventilation may be
✓ Monitor ABG levels for decreasing pH needed for patients who cannot
levels, as appropriate keep their oxygen saturation at
✓ Maintain patent IV access. 90% or who have respiratory
✓ MIO muscle fatigue
✓ Monitor determinants of tissue oxygen ✓ Preventing complications: is a
delivery (E.g. PaO2, SaO2 and major nursing responsibility
hemoglobin levels and cardiac output), ✓ Monitor breathing status and
if available intervene when changes occur are
✓ Monitor loss of bicarbonate through GI critical in preventing complications
tract (eg. diarrhea, pancreatic fistula,
small bowel fistula, and ileal conduit), ‣ For patients with chronic respiratory
as possible acidosis:
✓ Administer fluids as prescribed ✓ Assess breathing status at least 2
✓ Administer insulin and fluid hydration hours.
(Isotonic and hypotonic) for diabetic ✓ Listen to breath sounds and assess
ketoacidosis, causing metabolic how easily air moves into and out of
acidosis, as appropriate the lungs.
✓ Prepare patient for dialysis (eg. assist ✓ Check for any muscle retraction, the
with catheter placement for dialysis), as use of accessory muscles (especially
appropriate the neck muscles
✓ Institute seizure precaution [sternocleidomastoids] and whether
breathing produces a sound (like a
‣ Respiratory Acidosis: grunt or a wheeze)
aimed to maintain a patent airway and ✓ Assess the color of the nail beds and
enhance gas exchange oral membranes for cyanosis (a late
✓ These include: drug therapy, oxygen finding)
therapy, pulmonary hygiene
(positioning and breathing techniques), Metabolic acidosis
ventilatory support and prevention of (due to ⇣ in bicarbonate)
complications. Acidosis
Respiratory acidosis
✓ Drug therapy: such as bronchodilators; (due to ⇡ in carbonic acid)
Anti-inflammatories; Mucolytic
Metabolic alkalosis
✓ Oxygen therapy: helps promote gas
(due to ⇡ in bicarbonate)
exchange for patient with respiratory Alkalosis
acidosis Respiratory alkalosis
(due to ⇣ in carbonic acid)
Bulauitan Altered Fluid, Electrolyte 25 of 26
and Acid-Base Balance

- the pathologic effects are caused by

Alkalosis
the electrolyte imbalances that occur in
response to decreased blood cation
levels.
Pathophysiology: - Most problems of alkalosis are r/t
increased stimulation of the nervous,
neuromuscular and cardiac systems
In patient with alkalosis, the acid-base
balance of the blood is disturbed and has
an excess of bases, especially
Metabolic Alkalosis
bicarbonate (HCO3).

‣ Alkalosis: a decreased in free hydrogen Caused by conditions that create the acid-
ion level of the blood and is reflected by base imbalance through either an increase of
an arterial blood pH above 7.45 bases (base excess) or a decrease in acid
‣ Like acidosis, alkalosis is not a disease but, (acid deficit)
rather, a manifestation of a problem
caused by metabolic problems, respiratory ‣ Base excesses: are caused by excessive
problems, or both intake of bicarbonates, carbonates,
acetates, and citrates
Common Causes of Alkalosis ‣ Excessive use of oral antacids containing
sodium bicarbonate or calcium carbonate
‣ Metabolic Alkalosis: can also cause metabolic alkalosis
- Increased of base components ‣ Other base excesses can occur during
- Oral ingestion of bases: medical treatments such as citrate
Antacids; Milk-alkali syndrome excesses during massive blood
- Parenteral base administration: transfusions and IV sodium bicarbonate
Blood transfusions; Sodium given to correct acidosis.
bicarbonate; Total parenteral nutrition
- Decrease of acid components through: ‣ Acid Deficits: can be caused by disease
• Prolonged vomiting processes or medical treatment.
• Nasogastric suctioning - Disorders included prolonged
• Hypercortisolism vomiting, excess cortisol and
• Hyperaldosteronism hyperaldosteronism.
• Thiazide diuretics - Medical treatments that promote acid
loss causing metabolic alkalosis include
‣ Respiratory Alkalosis thiazide diuretics and prolonged
- Excessive loss of carbon dioxide nasogastric suctioning.
- Hyperventilation: due to Fear, anxiety;
mechanical ventilation; salicyclate
toxicity Respiratory Alkalosis
- Hypoxemia-stimulated hyperventilation
due to High altitude; shock; Early stage
is usually caused by an excessive loss of CO2
acute pulmonary problems
through hyperventilation (rapid respirations)

‣ Actual Bases excess alkalosis occurs when

bases (usually bicarbonate) is either
Assessment
overproduced or undereliminated.
‣ Relative Alkalosis the actual amount or
strength of bases does not increased, ‣ Many symptoms are the result of low
instead, the amount or strength (or both) calcium levels (hypocalcemia) and
of the acid decrease, thus creating an acid potassium levels (hypokalemia).
deficit making the blood more basic than ‣ These problems change the function of the
acidic. nervous neuromuscular, cardiac and
‣ Relative base-excess alkalosis (acid respiratory systems.
deficit) results from an over-elimination or
underproduction of acids
Bulauitan Altered Fluid, Electrolyte 26 of 26
and Acid-Base Balance

a) Central Nervous System Changes: ions; to restore fluid balance; to monitor

are caused by over-excitement of the changes
nervous systems, such as:
- Dizziness, agitation, confusion and I. Drug therapy
hyereflexia may progress to seizure
acitivty ‣ Fluid and electrolyte replacement given
- Tingling or numbness (parathesia) orally or parenterally
around the mouth and in the toes ‣ Antiemetic drugs
- Positive Chvostek’s and Trousseau’s ✓ Carefully monitor the patient’s
signs progress, and adjust fluid and
electrolyte therapy
b) Neuromuscular Changes ✓ Monitor serum electrolyte values daily
are related to the hypocalcemia and until they return to normal or near
hypokalemia that occur with alkalosis, normal
such as:
- Muscle cramps, twitches, and “charley Primary Secondary
Disorders pH [H+]
horses” Disturbances Response

- Deep tendon reflexes are hyperactive

- Tetany (continuous contractions) of
muscle groups, painful and indicates a
Metabolic
acidosis ↓ ↑ ↓ [HCO3] ↓ pCO2
rapidly worsening condition
- Skeletal muscle weakness:
- decrease handgrip strength
- the patient may be unable to stand
Metabolic
alkalosis ↑ ↓ ↑ [HCO3] ↑ pCO2
or walk

c) Cardiovascular Changes
occurs because alkalosis increases
Respiratory
acidosis ↓ ↑ ↑ pCO2 ↑[HCO3]
myocardial irritability, especially when
accompanied by hypokalemia
- Increased heart rate and a thready
pulse
Respiratory
alkalosis ↑ ↓ ↓ pCO2 ↑[HCO3]
- Severe hypotension
- Increased digitalis toxicity

d)Respiratory Changes
increased rate and depth of breathing
are the main causes of respiratory
alkalosis
- Respiratory efforts become less
effective as the skeletal muscle of
respiration weakens in metabolic
alkalosis

Laboratory and Diagnostic Test

‣ Arterial blood pH greater than 7.45,

confirms alkalosis
‣ Arterial blood gas (ABG) values and
specific serum electrolyte levels

Interventions

are planned to prevent further losses of

hydrogen, potassium, calcium and chloride