Download Chapter 15: Fluid and Electrolyte Balance Notes

Chapter 15: Fluids, Electrolytes, and Acid-Base Balance
Body Fluid Composition and Function
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Two body fluid compartments:
o Intracellular fluid (ICF)
 Consists of fluids within the cell cytoplasm and nucleus.
o Extracellular fluid (ECF)
 Fluid that exists outside the cell
 i.e. interstitial fluid between cells, fluid in the bloodstream, CSF, GI
secretion, sweat, and urine.
Osmolality
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The number of molecules of solute per kilogram of water.
Normal osmolality of blood is 275 to 295 miliosmoles per kilogram (mOsm/kg) of body weight.
o Fluids within this range are isotonic, above = hypertonic, below = hypotonic.
Electrolytes
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Electrolytes are ionized minerals (Na, K, Ca, Mg, P, Cl) that serve as energy transfer mechanisms
to power bodily functions using their ionic chemical properties.
o Cations (+) vs anions (-)
Regulation of Body Fluid
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Body fluids are regulated by:
o Osmosis
o Diffusion
o Filtration
 Takes place when molecules move from high concentration through a permeable
membrane to lower concentration as a result of hydrostatic pressure.
 Hydrostatic pressure – pressure exerted on the surrounding tissues
because of the presence of water.
 Oncotic pressure – result of the influence of plasma proteins on the
movement of water into and out of the blood stream.
Tests for Evaluating Fluid Status
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Osmolality of blood
Accumulation of ECF in the interstitial tissue especially in lower extremities or sacral region if
bed ridden.
Serum hematocrit
o Normal 40-50%
o Decreased if serum is diluted due to decreased values of:
 Na, K, Cl, HCO3.
Specific gravity: serum concentration indirectly calculated by measuring serum osmolality.
o Normal 1.015-1.024
o Low when blood is dilute; high when blood is concentrated.
Homeostatic Mechanisms
o Serum osmolality regulated by hypothalamus
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When 2% body water loss, hypothalamus stimulates posterior pituitary to secrete ADH.
 ADH signals kidneys to save water
 Thirst drive activated.
During severe dehydration (from vomiting), baroreceptors stimulate:
 ADH
 RAA system
Older Adults
 Atherosclerosis narrows renal and coronary arteries which stimulate the RAA
system which causes sodium and fluid retention without body water loss.
 ACE inhibitors and angiotensin-receptor blocking medications are used.
Clinical Manifestations of Overhydration and Dehydration
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If blood is dilute, water redistributes by osmosis to interstitial and ICF spaces causing cellular
edema.
o Cellular edema slows or interrupts normal cell functions because it swells the cell.
The most common cause of dehydration is excessive loss of water through urine.
o Occurs in diabetes insipidus, hyperglycemia (200+ mg/dL), diabetes mellitus, overuse of
diuretics, and if a person fails to drink enough fluids.
Nursing Management
o
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Assessing patient for S/S such as dizziness, headache, or syncope can be prevented with
adequate hydration.
o Overhydration in patients with CHF, may cause: dyspnea, SOB, and intolerance for
walking and other ADLs.
o Overhydration can lead to orthopnea (difficulty breathing when flat)
Electrolyte Balance
o Electrolyte balance is the sum of electrolyte intake, absorption, distribution, and
electrolyte loss through normal and abnormal routes.
 Intake mostly oral, may also be rectal (enemas) or IVs.
o Electrolyte distribution examples:
 Ca (bones and teeth), Potassium (intracellular compartment), Sodium and
Chloride (extracellular compartment)
o Most electrolytes lost via GI, GU, and sweat.
Electrolyte Imbalances
o Electromotive force (exchange of electrons between molecules)
 Body depends on this to or else electrolyte imbalances decrease the body’s ability
to act normally.
 Ie. Transmission of neural signals, contraction of muscles, secretion of
hormones, and regulation of normal body functions (oxygenation and
metabolization)
Sodium (Normal values: 135-145 mEq/L)
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Most abundant cation in the ECF.
o Maintains ECF with its osmotic pressure
o Regulates acid-base balance (combines with Cl and HCO3)
o Conducts nerve impulses (Sodium channels)
Three hormones regulate sodium levels in the ECF
o Aldosterone
 Secreted in response to low ECF sodium levels, increased ICF potassium, low
CO, and stress.
 Causes sodium reuptake from the kidney filtrate
o ADH
 Released in response to increased ECF osmolality (osmoreceptors in
hypothalamus)
 Causes reabsorption of water from kidney distal tubules.
o Atrial natriuretic peptide (ANP)
 Secreted by atrium of the heart.
 Secreted in response to excessive stretching of atrium by excessive ECF volume.
 Aldosterone antagonist: causes sodium excretion resulting in water loss and
lower blood volume.
Hypernatremia
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Occurs when excessive loss of body fluids,
o Ex, Cushing syndrome (aldosterone (sodium) excess) or diabetes insipidus (fluid loss)
S/S:
o Thirst, low fever, peripheral and pulmonary edema, and postural hypotension.
o A LOT, neuromuscular irritability, and occasionally coma or seizures.
Brain adjusts to ECF hypertonicity after 24hrs by moving excess ions and water into the brain
cells.
o Danger of IV fluids, fluid might move into cerebral cells and cause cerebral edema.
 Can lead to brain cell dysfunction, increased ICP.
Management:
o Care plan pg 353
o Risk for cerebral edema
o Sodium should be tapered off due to potential brain dysfunction w/ neuro problems.
Hyponatremia
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Causes:
o Excessive water retention, inadequate sodium intake, or loss of sodium fluids then
replace with pure water.
o Diuretics, vomiting, diarrhea, GI suctioning, excessive wound drainage.
o Excessive D5W IV causing more free water after the glucose is metabolized.
o Thiazide diuretics block sodium resorption
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S/S:
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S/s caused by cells reduced ability to depolarize and polarize.
Sodium levels below 120 mEq/L:
 Neuro changes: lethargy, headache, onfusion, personality changes, apprehension,
seizures, and even coma.
 Edema due to reduced osmotic pressure in the ECF.
o Sodium levels below 115 mEq/L or is corrected too rapidly
 CNS demyelination: flaccid paralysis, dysarthria, and dysphagia.
o SIADH
 Occurs as a result of (brain trauma, s/e of lithium, diuretics, or anticancer drugs)
that causes increased ADH secretion despite normal fluid volume.
 S/S:
 Bounding pulse, hypertension, pale dry skin, weight gain and edema,
renal failure, weakness, confusion, and possible seizures.
Management
o Return serum sodium levels to normal (135 mEq/L)
 Water intake restriction
 Foods high in sodium (processed foods, chips)
 Hypertonic saline IV (only in severe cases)
o Management Plan (pg 354)
Potassium
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Essential for cellular integrity, transmission of neuromuscular impulses, acid-base balance,
conversion of carbohydrates into energy, and the formation of amino acids into proteins.
Serum potassium affects the strength and rate of cardiac contraction.
Potassium is found in meat, potatoes, bananas and other foods.
o Since most foods contain Potassium, an increase in caloric intake is likely to increase
potassium intake.
When body is building new tissue, potassium is stored in the cells.
o Potassium moves into the blood when:
 Tissue injury or during starvation
 Periods of acidosis
Potassium is lost from the body in the kidneys via the GI tract (HCl buffer) and GU tract
(exchanged for sodium)
Hyperkalemia
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Causes:
o Increased/inappropriate K+ intake
o Renal disease
 Decreased urinary excretion
o Cellular injury
 Surgery, fever, sepsis, or trauma (mostly burns).
o Decreased potassium excretion
 May be a result of acute or chronic renal failure
 Potassium-sparing diuretics
o Severe acidosis
o Addison’s disease
 Decreased aldosterone secretion (decreased Na reuptake, increased K reuptake.
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S/S:
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Muscular weakness
Changes in ECG tracings
 Wide PR and QRS intervals
o Irregular pulse
o Irritability
o Abdominal distention
o Cramping
o Paresthesia
o Diarrhea
o ABGs may show metabolic acidosis
Management
o Assessment
 Signs and symptoms
 nutritional status
o Outcome and Evaluation Parameters
 Reduce cardiac risks within 6hr of admission
 HR within 60-120
 ECG normal rhythm (P wave, QRS within 0.12 seconds with normal
amplitude)
o Planning, Interventions, and Rationale
 Reduce K+ intake
 Treat any causes of hyperkalemia
 Administer potassium-reducing agent
 Kayexalate enemas are used to exchange K for Na in the GI
 Kayexalate oral combined with sorbitol pills reduce K+ by inducing
diarrhea
 Some drugs can temporarily lower potassium levels while the underlying cause is
being corrected:
 Calcium gluconate IV
 Concurrent dextrose 50% IV
 Beta-adrenergic blockers
 Sodium bicarbonate (if due to metabolic acidosis)
Hypokalemia
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When serum potassium is <3.5 mEq/L
o Average daily losses:
 5-10 mEq in feces
 0-20 mEq in sweat
 40-120 mEq in urine.
o Serum potassium not a true indicator of total body potassium loss because 90% of
potassium is in the cells.
Not usually a problem unless on non-potassium-sparing diuretics
Commonly associated with hypomagnesemia
Causes:
o Decreased K+ intake, GI and renal disorders, Cushing’s disease, K+ wasting diuretics,
and elevated serum insulin.
o Diarrhea increases excretion of potassium
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Vomiting or NG suction can increase potassium loss
Stress increases aldosterone as a response to elevated ADH
 Increased Na retention = decreased K retention
Management
o Assess the S/S:
 Muscle weakness, cramps, N/V, decreased bowel sounds (possible ileus
paralysis), paresthesia.
 Weak, irregular pulse
 Flattened T wave follow by a U wave.
 Ventricular ectopy due to slow repolarization of myocardium and could lea to
dysrhythmias.
o Planning, Interventions, and Rationales
 Treat underlying cause first
 Proper nutrition
 Potassium supplementation (PO or IV)
 Continue monitoring ECG when supplementation is given.
Calcium
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Important for neuromuscular transmission, contraction of muscles, blood clotting, bone and tooth
construction, cellular membrane function, and energy conversion.
Cellular membrane stability relies on calcium
Also has a sedative effect on nerves.
Serum pH greatly affects the levels of ionized calcium.
o Metabolic acidosis decreases Ca binding to albumin and causes it to ionize.
o Metabolic alkalosis does the opposite, causing tetany and muscle cramping to occur.
In the bone, Ca combines with P to form hydroxyapatite (inorganic hexagonal matrix of bone)
Serum calcium levels are controlled by:
o Vitamin D
 Essential for absorption of Ca and P from GI.
o Calcitonin (thyroid gland)
 Inhibits Ca resorption, causes deposition of Ca in bones and teeth.
 Increases Ca excretion
o Parathyroid hormone (PTH)
 Mobilizes Ca from the bones and increases Ca reabsorption by the kidneys.
Hypercalcemia
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Serum calcium > 5.25 mg/dL
Causes:
o Hyperparathyroidism
 Mobilizes Ca out of bones, increases reabsorption of Ca by kidneys
o Bone Malignancy
o Thiazide diuretics
 Vitamins A and D promote absorption of Ca from GI tract.
o Prolonged bed rest
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Management
o Treat underlying cause first
 Parathyroidectomy
 Chemo
 D/c of vitamins A and D, supplements, thiazide diuretics
o Assessment
 I/O prevent fluid overload and adequate kidney function.
 Monitor bone stability /t calcium mobilization from bones
 Auscultate for crackles and rhonchi
 Auscultate for development of S3 heart sound (may indicated fluid overload)
o Planning, Interventions, and Rationales
 NS administered rapidly concurrently with furosemide to dilute blood and
increase calcium secretion
 Biphosphonates inhibit osteoclast function.
 Glucocorticoids may be given to compete with Vitamin D and decrease calcium
absorption.
 Most effective in hematologic malignancies (multiple myeloma or
Hodgkin’s)
 Calcitonin to promote calcium deposition in bone and increase calcium excretion
 Gallium nitrate: inhibit malignancy-related bone resorption.
 *Special consideration: monitor patient if on digitalis to avoid toxicity*
Hypocalcemia
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Serum Ca level <9.0mg/dL; ionized Ca levels <4.25mg/dL
Causes:
o Infusion of large volume of citrated blood (citrate combines with calcium)
o Reduced calcium intake or absorption (Vitamin D deficiency or excessive P intake)
 Vitamin D deficiency most common cause; also causes rickets and osteomalacia
 Caused by:
o GI surgery, chronic pancreatitis, and small-bowel disease.
o Decreased PTH
 Damage or removed parathyroid gland
o Elevated serum phosphorus
o Decreased Mg levels
o Hypoalbuminemia
o Alkalosis
o Renal failure (excessive Ca loss by reducing P excretion)
o Loop diuretics
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S/S:
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Acute symptoms: changes in ECG (prolong QT intervals), cardiac contractility that may
progress to CHF, dysrhythmias, bradycardia, hypotension.
 Numbness and tingling of hands and fingers
 Hyperactive reflexes, muscle cramps, laryngeal spasm, bronchospasm, muscle
tetany, confusion, hallucinations, possible tonic-clonic seizures.
 Anxiety, depression, or psychosis.
 Pathologic fractures may occur due to weak bones.
 Trousseau’s sign (carpopdeal spasm)
 Inflating BP cuff 20mm above systolic and maintaining for 3 minutes
o Causing wrist and fingers to contract inward.
 Chvostek’s sign
 Twitching of the facial muscles by tapping facial nerve.
 Laryngeal spasm can occur with severe hypocalcemia resulting in asphyxiation.
Management
o Treatment:
 Oral or IV administration of Ca.
 Monitor Phosphorus levels to r/o hyperphosphatemia.
 Elevated levels of Ca and P produces precipitates in the blood vessels
which result in tissue ischemia called calciphylaxis.
 Rapid admin of Ca can result in cardiac arrest or hypotension.
 Calcium gluconate better than CaCl because less irritating to veins.
 Should not be infused at rate > than 60
 Longer therapy
 Vitamin D
 Phosphate-binding antacids may be given to reduce P and increase Ca
o Taken with meals
 Oral Ca and vitamin D supplements for chronic hypocalcemia
o Taken 30 min before a.c for maximum absorption.
Magnesium
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More than 50% store in muscle and bone.
Body requirement 4.5mg/kg
Kidney disease decreases Mg absorption due to inactive vitamin D.
ETOH decreases renal MG reabsorption.
Hypermagnesemia
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May occur with renal failure, adrenal insufficiency, or IV-induced (treatment of PIH)
S/S similar to hyperkalemia:
o Hypotension, bradycardia, flushing and warmth, possible respiratory (lost at 10mg) or
cardiac arrest (>15mg)
o N/V, drowsiness, respiratory depression, and decreased deep tendon reflex (lost at 8mg),
and coma (10mg).
Management
o Assessment of tendon reflex, respiratory status.
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Treatment: immediate cessation of Mg-containing products, IV push of calcium
gluconate, or dialysis.
NS with diuretics to promote renal excretion.
Hypomagnesemia (<1.8mg/dL)
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Causes:
o Malnutrition
o Urinary excretion r/t alcoholism, osmotic diuresis in DM, or loop diuretics.
o GI loss (vomiting, diarrhea, malabsorption syndrome)
o Associated with other electrolytes such as K and Ca.
S/S
o Severe: confusion, lethargy, seizures, hyperreflexia of deep tendon reflexes, tetany,
hallucinations, n/v, hypertension, cardiac dysrhythmias, and death.
o Supraventricular tachycardia, possible coronary artery spasms, and paresthesia.
Management:
o Parenteral and/or PO magnesium supplements. Severe cases IV.
Phosphorus
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About 500-1600mg/day absorbed with help of vitamin D.
Body’s basic energy units (ADP/ATP), cell membranes (phospholipids),nasoc imot pf a jpr,pme
fpimd om RBC’s to increase amount of O2 they can carry.
Regulated by calcitonin, PTH (blocks reabsorption), and vitamin D in conjunction with Ca
regulation.
Primarily regulated by the kidneys.
Ca reabsorbed = P excreted
Glucose or insulin temporarily shifts Phosphorus into the cells.
Hyperphosphatemia (>4.5mg/dL)
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Causes:
o Renal disease (decreased excretion)
o Excessive phosphate replacement or enemas
o Acidosis may cause ECF shift
o Cellular destruction
 Malignancy, chemo, radiation, rhabdomyolysis
Complications
o Deposition of calcium phosphate in soft tissues.
 Deposition in the heart can result in cardiac dysrhythmias
 Most S/S are related to hypocalcemia not hyperpohsphatemia.
Management
o Administration of phosphorus-binding antacids: calcium carbonate or calcium acetate.
o Decrease P absorption, increase excretion.
o Calcium-based antacids preferred for renal failure to avoid hypermagnesemia.
o Hyperphosphatemia accompanied by hypocalcemia so correcting Ca levels may work.
Hypophosphatemia (<2.5mg/dL)
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Causes:
o Vitamin D deficiency (alcoholics)
o Bowel disorders that lead to malabsorption
o Excessive phosphate-binding antacids
o DKA (taken up as a buffer)
o Elevated PTH (kidney may not reabsorb phosphorus)
S/S:
o S/S are mostly due to decreased availability of ADP and reduced O2 capacity of RBC’s.
o Metabolic encephalopathy syndrome may occur (irritable, confused, seizures, or chest
pain)
o Respiratory failure possible (muscle weakness and diaphragm dysfunction)
o Patients with respiratory weakness (monitor phosphate levels)
o Neuro symptoms: apathy, delirium, hallucinations, and paranoia.
o Bone weakness and pathologic fractures.
o Peripheral neuropathy and ascending motor paralysis.
 Guillaine-Baree syndrome
o Extrapontine myelinolysis (osmotic demyelination)
o Hemolytic anemia (erythrocyte destruction in the spleen)
 Compromised o2 delivery to tissues
 Leads to hypoxia, cardiac dysrhythmia, and heart block.
Management:
o Treatment:
 Treat underlying cause first
 High phosphate diet: beans, peas, eggs, fish, organ meats, nuts, poultry, seeds,
and whole grains.
 Oral Phosphate supplements can be taken.
 IV phosphate not indicated due to risk of hyper which will cause hypocalcemia.
Chloride
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Assists in reabsorption of Na.
Used as HCL in GI tract, also used as buffer in alkalosis and acidosis.
The anion gap is based on the principle of electroneutrality where the (+/-) charges must all be
equal.
o Normal (10-17), anything above 30 indicated excess organic acid (lactic acid or ketones)
Hyperchloremia (>105mEq/L)
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Causes:
o Metabolic acidosis
o Hyperparathyroidism
o Dehydration
o Respiratory alkalosis
S/S:
o Increased depth and rate of respiration, lethargy, stupor, disorientation, and coma (if
acidosis not treated).
Treatment:
o Treat underlying cause
o NS to repair volume loss only and administration of K
Hypochloremia (<95 mEq/L)
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Cause:
o Loss of GI fluids (HCL)
o Stomach pyloric obstruction r/t duodenal ulcer or prolonged vomiting secondary to bowel
obstruction.
o DKA may cause increase in HCO3 resulting in Cl los.
o Bartter’s syndrome: prevents Cl reabsorption.
Hypochloremia may cay cause acidosis because bicarbonate will be retained to maintain
electroneutrality (both are negative Cl- vs HCO3-)
S/S:
o Paresthesias of the face and extremities, muscle spasms, tetany, slow and shallow
respirations, and dehydration.
Treatment:
o IV fluids preferably NS 0.9%