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Fluid and Electrolytes
Body Fluids and Fluid
Compartments
• The percentage of total body water: 45-75%
• Intracellular compartment
– 2/3 of body water (40% body weight)
• Extracellular compartment
– 1/3 of body water (20% body weight)
– the blood plasma (water=4.5% body weight)
– interstitial fluid and lymph (water=15% body
weight)
– transcellular fluids: e.g. cerebrospinal fluid,
aqueous humor (1.5% BW)
Body Water Distribution
Input
RBC
PLASMA WATER
5%
3L
ECF
20%
CELL WATER
40%
28 L
INTERSTITIAL
FLUID
COMPARTMENT
15%
10 L
TRANSCELLULAR WATER
1%
1L
14 L
Body Water Content
• Infants have low body fat, low bone mass, and
are 73% or more water
• Total water content declines throughout life
• Healthy males are about 60% water; healthy
females are around 50%
• This difference reflects females’:
– Higher body fat
– Smaller amount of skeletal muscle
• In old age, only about 45% of body weight is
water
Fluid Compartments
Intracellular fluid (ICF)
Two thirds by volume, contained in cells
Extracellular fluid (ECF)
Two major subdivisions
– Plasma – the fluid portion of the blood
– Interstitial fluid (IF) – fluid in spaces between cells
Other ECF –
• lymph, cerebrospinal fluid, eye humors, synovial
fluid, serous fluid, and gastrointestinal secretions
Fluid Compartments
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• Fluid compartments are separated by
membranes that are freely permeable to
water.
• Movement of fluids due to:
– hydrostatic pressure
– osmotic pressure
• Capillary filtration (hydrostatic) pressure
• Capillary colloid osmotic pressure
• Interstitial hydrostatic pressure
• Tissue colloid osmotic pressure
Balance
• Fluid and electrolyte homeostasis is
maintained in the body
• Neutral balance: input = output
• Positive balance: input > output
• Negative balance: input < output
Water Balance and ECF Osmolality
• Water intake sources
– Ingested fluid (60%) and solid food (30%)
– Metabolic water or water of oxidation (10%)
• Water output
– Urine (60%) and feces (4%)
– Insensible losses (28%), sweat (8%)
• Increases in plasma osmolality trigger thirst
and release of antidiuretic hormone (ADH)
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Water Steady State
• Amount Ingested = Amount Eliminated
• Pathological losses
vascular bleeding (H20, Na+)
vomiting (H20, H+)
diarrhea (H20, HCO3-).
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Principles of Body Water
Distribution
• Constant total body water
• Constant total body osmolarity
• Osmolarity is identical in all body fluid
compartments (steady state conditions)
– Body water will redistribute itself as
necessary to accomplish this
Disorders of Water Balance:
Hypotonic Hydration
1
Excessive H2O enters
the ECF
(b) Mechanism of hypotonic hydration
2
ECF osmotic
pressure falls
3 H2O moves into
cells by osmosis;
cells swell
Disorders of Water Balance:
Hypotonic Hydration
• Renal insufficiency or an extraordinary amount
of water ingested quickly can lead to cellular
overhydration, or water intoxication
• ECF is diluted – sodium content is normal but
excess water is present
• The resulting hyponatremia promotes net
osmosis into tissue cells, causing swelling
• These events must be quickly reversed to
prevent severe metabolic disturbances,
particularly in neurons
Disorders of Water Balance: Dehydration
1 Excessive loss of H2O from
ECF
2
ECF osmotic
pressure rises
3 Cells lose H2O
to ECF by
osmosis; cells
shrink
(a) Mechanism of dehydration
Figure 26.7a
Response
- Renal sympathetic nerve activity
- Intrarenal blood flow distribution
- Plasma atrial natriuretic factor (ANF)
-Aldosterone
-Renin-Angiotensin system
-release of renin
-renin formation of angiotensin II
- angiotensin II:
-
blood pressure
-
synthesis and release of aldosterone;
-
stimulation of the hypothalamic thirst centers;
-
release of ADH
Too Much
Response
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Atrial Natriuretic Peptide (ANP)
Net reabsorption of salt and water occurs at proximal
convoluted tubule

peritubular capillary hydrostatic forces

colloid osmotic pressure
Atrial natriuretic peptide

Released in response to an increase in blood volume (distention atria)
Release of (ANP)

increase sodium excretion by increasing GFR and inhibiting sodium
reabsorption
• Atrial natriuretic peptide
Too Little
Principal cells & aldosterone
• Decreased blood pressure stimulates
renin secretion
Pathway of RAAS
Influence and Regulation of ADH
• Hypothalamic osmoreceptors trigger or inhibit ADH
release
• ADH release trigger prolonged fever; excessive sweating,
vomiting, or diarrhea; severe blood loss; and traumatic
burns
• Water reabsorption in collecting ducts is proportional to
ADH release
• Low ADH levels produce dilute urine and reduced volume
of body fluids
• High ADH levels produce concentrated urine
Mechanisms and Consequences of ADH Release
Clinical relevance
Too little
• malperfusion
• Shock
Too Much
• Malperfusion
• Shock
• Edema Pulmonay hepatic systemic
• Heart arrythmias
• Heart failure
Edema is the accumulation of fluid within the
interstitial spaces.
Causes:
increased hydrostatic pressure
lowered plasma osmotic pressure
increased capillary membrane permeability
lymphatic channel obstruction
Decreased plasma osmotic pressure:
↓ plasma albumin (liver disease or
protein malnutrition)
plasma proteins lost in :
glomerular diseases of kidney
hemorrhage, burns, open wounds
and cirrhosis of liver
Increased capillary permeability:
Inflammation
immune responses
Fluid accumulation:
increases distance for diffusion
may impair blood flow
= slower healing
increased risk of infection
pressure sores over bony
prominences
Continuous Mixing of Body Fluids
Continuous mixing yet body fluids are:
– Electrically neutral
– Osmotically maintained
• Specific number of particles per volume
of fluid
Water Intake and Output
Movement of fluids
Where sodium goes, water follows
Diffusion – Movement of particles down a
concentration gradient.
Osmosis – Diffusion of water across a
selectively permeable membrane
Active transport – Movement of particles up
a concentration gradient ; requires energy
Solutes – dissolved particles
• Electrolytes – charged particles
– Cations – positively charged ions
• Na+, K+ , Ca++, H+
– Anions – negatively charged ions
• Cl-, HCO3- , PO43-
• Non-electrolytes - Uncharged
• Proteins, urea, glucose, O2, CO2
Electrolyte (Na+, K+, Ca++) Steady
State
• Amount Ingested = Amount Excreted.
• Normal entry: Mainly ingestion in food.
• Clinical entry: Enteral and parenteral
Composition of Body Fluids
• Water the universal solvent
• Solutes broadly classified into:
– Electrolytes – inorganic salts, all acids and bases,
and some proteins
– Nonelectrolytes – examples include glucose, lipids,
creatinine, and urea
• Electrolytes have greater osmotic power than
nonelectrolytes
Electrochemical Equivalence
• Equivalent (Eq/L) = moles x valence
• Monovalent Ions (Na+, K+, Cl-):
– 1 milliequivalent (mEq/L) = 1 millimole
• Divalent Ions (Ca++, Mg++, and HPO42-)
– 1 milliequivalent = 0.5 millimole
Extracellular and Intracellular Fluids
• Each fluid compartment has a set pattern of
electrolytes
• All Extracellular fluids are similar (except for the
high protein content of plasma)
– Sodium is the chief cation
– Chloride is the major anion
• In general intracellular fluids have low sodium
and chloride
– Potassium is the chief cation
– Phosphate is the chief anion
Extracellular and Intracellular Fluids
• Sodium and potassium concentrations in
extra- and intracellular fluids are nearly
opposites
• This reflects the activity of cellular ATPdependent sodium-potassium pumps
• Electrolytes determine the chemical and
physical reactions of fluids
Summary of Ionic composition
Protein
Organic Phos.
Inorganic Phos.
Bicarbonate
Chloride
Magnesium
Calcium
Potassium
Sodium
400
300
200
100
0
Plasma
H2O
Interstitial
H2O
Cell
H2O
Regulation of Anions
• Chloride is the major anion accompanying
sodium in the ECF
• 99% of chloride is reabsorbed under normal
pH conditions
• When acidosis occurs, fewer chloride ions are
reabsorbed
• Other anions have transport maximums and
excesses are excreted in urine
Electrolyte balance
• Na + (Sodium)
– 90 % of total ECF cations
– 136 -145 mEq / L
– Pairs with Cl- , HCO3- to neutralize charge
– Low in ICF
– Most important ion in regulating water balance
– Important in nerve and muscle function
Regulation of Sodium
• Renal tubule reabsorption affected by
hormones:
– Aldosterone
– Renin/angiotensin
– Atrial Natriuretic Peptide (ANP)
Electrolyte imbalances: Sodium
• Hypernatremia (high levels of sodium)
– Plasma Na+ > 145 mEq / L
– Due to ↑ Na + or ↓ water
– Water moves from ICF → ECF
– Cells dehydrate
– Free water deficit
• 0.6 x patient’s weight in kg x (patient’s sodium/140 - 1)
Hypernatremia
The regulated variable affecting sodium
excretion is effective arterial blood volume
Changes in effective arterial blood volume can
elicit the appropriate renal response by three
possible mechanisms
change in blood volume  glomerular blood flow
and capillary pressure  GFR
a
 a change in blood volume detected by an
intrarenal baroreceptor  release of renin
 a change in blood volume could change
peritubular capillary Starling forces
Other factors affecting sodium excretion include:

glucocorticoids
 estrogen
 osmotic diuretics
 poorly reabsorbed anions
 diuretic drugs
• Hypernatremia Due to:
– Hypertonic IV soln.
– Oversecretion of aldosterone
– Loss of pure water
• Long term sweating with chronic fever
• Respiratory infection → water vapor loss
• Diabetes – polyuria
– Insufficient intake of water (hypodipsia)
Clinical manifestations
of Hypernatremia
• Thirst
• Lethargy
• Neurological dysfunction due to dehydration
of brain cells
• Decreased vascular volume
Treatment of Hypernatremia
• Lower serum Na+
– Stop Na loading
– Isotonic salt-free IV fluid
– Slow reduction
– rate of 0.5 to 1 mEq/h with a decrease of no more than
approximately 12 mEq/L in the first 24 hours and the remainder
over the next 48 to 72 hours
– Change in serum Na per liter = Infusate Na – Serum Na / weight in
Kg x 0.6 -1
– Oral solutions preferable
– Oral (FT) may not be well tolerated
• Aspiration risk NG
Hyponatremia
• Overall decrease in Na+ in ECF
• Two types: depletional and dilutional
• Depletional Hyponatremia
Na+ loss:
– diuretics, chronic vomiting
– Chronic diarrhea
– Decreased aldosterone
– Decreased Na+ intake
• Dilutional Hyponatremia:
– Renal dysfunction with ↑ intake of hypotonic
fluids
– Excessive sweating→ increased thirst → intake of
excessive amounts of pure water
– Syndrome of Inappropriate ADH (SIADH) or
oliguric renal failure, severe congestive heart
failure, cirrhosis all lead to:
• Impaired renal excretion of water
– Hyperglycemia – attracts water
Clinical manifestations of
Hyponatremia
• Neurological symptoms
– Lethargy, headache, confusion, apprehension,
depressed reflexes, seizures and coma
• Muscle symptoms
– Cramps, weakness, fatigue
• Gastrointestinal symptoms
– Nausea, vomiting, abdominal cramps, and diarrhea
Treatment of Hypernatremia
• Gradual typically increase the Na+ by 0.5
mEq/L per hour to a maximum change of
about 12 mEq/L in the first 24 hours
– central pontine myelinolysis
• Fluid restrict
– 50% to 66% of estimated maintenance fluid
requirement
Hyponatremia Neurologic Compromise
• 3% saline IV immediately to correct (raise) the serum
sodium at a rate of 1 mEq/L per hour until neurologic
symptoms are controlled
• Some recommend a faster rate of correction (ie,
increase concentration 2 to 4 mEq/L per hour) when
seizures are present
• Na+ deficit=(desired [Na+]–current [Na+])x0.6*x
body wt (kg) (*use 0.6 for men and 0.5 for women).
determine the volume of 3% saline divide the deficit
(513 mEq/L Na+)
Potassium
•
•
•
•
•
Major intracellular cation
ICF conc. = 150- 160 mEq/ L
Resting membrane potential
Regulates fluid, ion balance inside cell
pH balance
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Regulation of Potassium
• Through kidney
– Aldosterone
– Insulin/ glucose economy
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Influence of Plasma Potassium Concentration
• High K+ content of ECF favors principal cells to
secrete K+
• Low K+ or accelerated K+ loss depresses its
secretion by the collecting ducts
Influence of Aldosterone
• Aldosterone stimulates potassium ion
secretion by principal cells
• In cortical collecting ducts, for each Na+
reabsorbed, a K+ is secreted
• Increased K+ in the ECF around the adrenal
cortex causes:
– Release of aldosterone
– Potassium secretion
• Potassium controls its own ECF concentration
via feedback regulation of aldosterone release
Hypokalemia
• Serum K+ < 3.5 mEq /L
• Beware if diabetic
– Insulin gets K+ into cell
– Ketoacidosis – H+ replaces K+, which is lost
in urine
• β – adrenergic drugs or epinephrine
Causes of Hypokalemia
• Decreased intake of K+
• Increased K+ loss
– Chronic diuretics
– Acid/base imbalance
– Trauma and stress
– Increased aldosterone
– Redistribution between ICF and ECF
Clinical manifestations of Hypokalemia
• Call from Nurse/ Lab
• Neuromuscular disorders
– Weakness, flaccid paralysis, respiratory
arrest, constipation
• Dysrhythmias, appearance of U wave
• Postural hypotension
• Cardiac arrest
• Treatment– Increase K+
Hyperkalemia
• Serum K+ > 5.5 mEq / L
Causes
• Renal disease
• Massive cellular trauma
• Insulin deficiency
• Addison’s disease
• Potassium sparing diuretics
• Decreased blood pH
Clinical manifestations of
Hyperkalemia
•
•
•
•
•
•
Call from Nurse/ Lab
Early – hyperactive muscles , paresthesia
Late - Muscle weakness, flaccid paralysis
Change in ECG pattern
Dysrhythmias
Bradycardia , heart block, cardiac arrest
Treatment of Hyperkalemia
•
•
•
•
Decrease intake and increase renal excretion
Insulin + glucose
Bicarbonate
Ca++ counters effect on heart
AHA Guidelines
Elevation 5 to 6 mEq/L
• Diuretics: furosemide 40 to 80 mg IV
• Resins: Kayexalate 15 to 30 g in 50 to 100 mL
of 20% sorbitol either orally or by retention
enema
6 to 7 mEq/L
• Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10
U regular insulin and give IV over 15 to 30 minutes
• Sodium bicarbonate: 50 mEq IV over 5 minutes
– sodium bicarbonate alone is less effective than glucose plus insulin
or nebulized albuterol, particularly for treatment of patients with
renal failure; it is best used in conjunction with these medications
• Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes
>7 mEq/L with toxic ECG changes
• Shift potassium into cells:
• Calcium chloride (10%): 500 to 1000 mg (5 to 10 mL) IV over 2 to 5 minutes to
reduce the effects of potassium at the myocardial cell membrane (lowers risk of
ventricular fibrillation [VF])
• Sodium bicarbonate: 50 mEq IV over 5 minutes (may be less effective for patients
with end-stage renal disease)
• Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10 U regular insulin and
give IV over 15 to 30 minutes
• Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes
•
• Promote potassium excretion:
– 5. Diuresis: furosemide 40 to 80 mg IV
– 6. Kayexalate enema: 15 to 50 g plus sorbitol PO or per rectum
– 7. Dialysis
Calcium Imbalances
• Most in ECF
• Regulated by:
– Parathyroid hormone
• ↑Blood Ca++ by stimulating osteoclasts
• ↑GI absorption and renal retention
– Calcitonin from the thyroid gland
• Promotes bone formation
• ↑ renal excretion
Hypercalcemia
• Results from:
– Hyperparathyroidism
– Hypothyroid states
– Renal disease
– Excessive intake of vitamin D
– Milk-alkali syndrome
– Certain drugs
– Malignant tumors – hypercalcemia of malignancy
• Tumor products promote bone breakdown
• Tumor growth in bone causing Ca++ release
Hypercalcemia
• Usually also hypophosphatemia
• Effects:
– Many nonspecific – fatigue, weakness, lethargy
– Increases formation of kidney stones and pancreatic
stones
– Muscle cramps
– Bradycardia, cardiac arrest
– Pain
– GI activity also common
• Nausea, abdominal cramps
• Diarrhea / constipation
– Metastatic calcification
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Hypocalcemia
• Hyperactive neuromuscular reflexes and tetany
differentiate it from hypercalcemia
• Convulsions in severe cases
• Caused by:
– Renal failure
– Lack of vitamin D
– Suppression of parathyroid function
– Hypersecretion of calcitonin
– Malabsorption states
– Abnormal intestinal acidity and acid/ base bal.
– Widespread infection or peritoneal inflammation
Hypocalcemia
• Diagnosis:
– Chvostek’s sign
– Trousseau’s sign
• Treatment
– IV calcium for acute
– Oral calcium and vitamin D for chronic
Regulation of Calcium
• Ionic calcium in ECF is important for:
– Blood clotting
– Cell membrane permeability
– Secretory behavior
• Hypocalcemia:
– Increases excitability
– Causes muscle tetany
Regulation of Calcium
• Hypercalcemia:
– Inhibits neurons and muscle cells
– May cause heart arrhythmias
• Calcium balance is controlled by parathyroid
hormone (PTH) and calcitonin
Regulation of Calcium and Phosphate
• PTH promotes increase in calcium levels by
targeting:
– Bones – PTH activates osteoclasts to break down
bone matrix
– Small intestine – PTH enhances intestinal
absorption of calcium
– Kidneys – PTH enhances calcium reabsorption and
decreases phosphate reabsorption
• Calcium reabsorption and phosphate
excretion go hand in hand
Regulation of Calcium and Phosphate
• Filtered phosphate is actively reabsorbed in the
proximal tubules
• In the absence of PTH, phosphate reabsorption
is regulated by its transport maximum and
excesses are excreted in urine
• High or normal ECF calcium levels inhibit PTH
secretion
– Release of calcium from bone is inhibited
– Larger amounts of calcium are lost in feces and urine
– More phosphate is retained
Influence of Calcitonin
• Released in response to rising blood calcium
levels
• Calcitonin is a PTH antagonist, but its
contribution to calcium and phosphate
homeostasis is minor to negligible