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Base Balance
Michael Jenifer RN, MSN
Pathophysiology
Overview
Cellular fluid
2/3 of TBW
Interstitial fluid
Between cells & outside vessels
Fat is hydrophobic
Pediatrics
75% to 80% of body weight
Susceptible to significant changes in
body fluids
Dehydration in newborns
Aging
Decreased percent of total body water
Body Fluids
Water sources
Drinking, food water & by product of oxidative
metabolism
Water excretion
Renal, stool & vaporization of skin & lungs
Infants
High water weight & immature kidneys
Elderly
Decreased fat masses, decreased muscle mass
& decreased renal efficiency
Diminished thirst perception
Water Movement
Osmosis
Movement of water through a semi permeable
membrane from a region of higher
concentration to one of lower concentration
Water Movement
Net Filtration
Edema
Thrombophlebitis
Hepatic obstruction
Tight clothing
Prolonged standing
Heart & renal failure
Neoplastic disease
Allergic reactions
Surgical removal
Inflammation
Tumors
Localized
Usually limited to site of trauma
Organ edema
Generalized
More uniform distribution in interstitial
space
Dependent edema
Sodium
Primary ECF cation
Regulates osmotic forces, thus water
Roles
Chloride
Primary ECF anion
Provides electroneutrality
Sodium
90% of ECF cations
Partners with anions chloride & bicarbonate to
control osmotic forces
Works with potassium & calcium to maintain
irritability & acid base balance
Chloride
Major anion in ECF
Inverse concentration relationship with HCO3
Natriuretic hormones
Promote excretion of Na
Water Balance
Renin-angiotensin-aldosterone
system
Aldosteroneleads to sodium and
water reabsorption back into the
circulation and potassium and
hydrogen secretion to be lost in
urine
Natriuretic peptides
Renin-Angiotensin-Aldosterone System
Electrolyte Distribution
ECF
142
5
5
2
154
24
104
2
16
8
154
Cations
ICF
10
156
4
26
196
Na
K
Ca
Mg
Totals
Anions
Bicarb
12
Chloride
4
Phosphate 100
Proteins
54
Others
6
Totals
176
Excessive NS
Hypersecretion of aldosterone which leads
to retention of Na & water
Corticosteroids
Hypertonic Alterations
Hypernatremia
Clinical Problems
Thirst
Fever
Dry mucous membranes
Restlessness
CNS twitching
Hyperreflexia
Convulsions & pulmonary edema are late
problems if untreated
Will see concentrated urine & S & S of
hypovolemia with water deficits
Hypotonic Alterations
Hypotonic IVs
Large water intake
Impaired water excretion
Osmotic shifts
Hyponatremia
Clinical Problems
Lethargy
Confusion
Apprehension
Depressed reflexes
Seizures
Coma
Will see hypovolemia S & S with Na loss
Will see weight gain & JVD with dilutional
Water Excess
Potassium
Hypokalemia
K is < 3.5mEq/L
Generally a low serum K means total K
depletion
Causes
Magnesium deficits
Hypokalemia
Clinical Problems
None if mild
Decreased neuromuscular excitability
Hyperkalemia
Hyperkalemia
Clinical Problems
Vary with severity
Neuromuscular
EKG Effects
Cardiac Effects of K
Potassium Levels
Calcium
Phosphate
Hypocalcemia
Causes:
Inadequate intestinal absorption, deposition of
ionized calcium into bone or soft tissue, blood
administration
Decreases in PTH and vitamin D
Nutritional deficiencies occur with inadequate
sources of dairy products or green leafy vegetables
Effects:
Increased neuromuscular excitability
Hypercalcemia
Causes:
(contd)
Hyperparathyroidism
Bone metastases with calcium resorption from breast,
prostate, renal, and cervical cancer
Sarcoidosis
Excess vitamin D
Many tumors that produce PTH
Effects:
Phosphate
Hypophosphatemia
Causes:
Intestinal
malabsorption
(vitamin D deficiency,
use of magnesiumand aluminumcontaining antacids,
long-term alcohol
abuse);
Malabsorption
syndromes
Respiratory alkalosis
Increased renal
excretion of
phosphate associated
with
hyperparathyroidism
Effects:
Hyperphosphatemia (contd)
Causes:
Acute or chronic renal
failure with significant
loss of glomerular
filtration
Treatment of
metastatic tumors
with chemotherapy
that releases large
amounts of phosphate
into serum
Long-term use of
laxatives or enemas
containing phosphates
Hypoparathyroidism
Effects:
Symptoms primarily
related to low serum
calcium levels (caused
by high phosphate
levels) similar to the
results of hypocalcemia
When prolonged,
calcification of soft
tissues in lungs,
kidneys, joints
Magnesium
Intracellular cation
Plasma concentration is 1.8 to 2.4
mEq/L
Acts as a cofactor in intracellular
enzymatic reactions
Increases neuromuscular
excitability
Hypomagnesemia
Causes:
Malnutrition,
Malabsorption
syndromes
Alcoholism
Urinary losses
(renal tubular
dysfunction,
loop diuretics)
Effects:
Behavioral
changes
Irritability
Increased reflexes
Muscle cramps
Ataxia
Nystagmus
Tetany
Convulsions
Tachycardia
Hypotension
Hypermagnesemia
Causes:
Usually renal insufficiency or failure
Also excessive intake of magnesium-containing antacids
Adrenal insufficiency
Effects:
Acid-Base Balance
pH (contd)
pH (contd)
pH (contd)
Nonvolatile
Hydrogen & pH
Buffer Systems
Buffering Systems
Renal buffering
Secretion of H+ in the urine and
reabsorption of HCO3
Protein buffering
Proteins have negative charges, so
they can serve as buffers for H+
Renal buffering
Secretion of H+ in the urine and
reabsorption of HCO3
Acid-Base Imbalances
7.35 to 7.45
Obtained by arterial blood gas (ABG)
sampling
Acidosis
Alkalosis
Systemic decrease in H+
concentration or increase in
bicarbonate
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
Davenport Diagram
Clinical Problems in
Metabolic Acidosis
H/A, lethargy, Kussmaul
respiration, anorexia, N/V,
abdominal discomfort
Leads to coma & death
Clinical Problems in
Respiratory Acidosis
Restlessness,
disorientation, muscle
twitching, tremors, warm
skin due to vasodilation
Rapid RR leading to
depression
Clinical Problems in
Metabolic Alkalosis
Weakness, cramps,
hyperactive reflexes,
tetany, shallow/slow RR,
confusion, convulsions,
atrial tach
Clinical Problems in
Respiratory Alkalosis
Dizziness, confusion,
tingling in extremities,
convulsions & coma
Reduced cerebral blood
flow due to
vasoconstriction
Case Study