Chapter 3
The Cellular Environment: Fluids
and Electrolytes, Acids and Bases
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Distribution of Body Fluids

Total body water (TBW)


Intracellular fluid
Extracellular fluid
• Interstitial fluid
• Intravascular fluid
• Lymph, synovial, intestinal, biliary, hepatic, pancreatic,
CSF, sweat, urine, pleural, peritoneal, pericardial, and
intraocular fluids
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Water Movement Between
the ICF and ECF




Osmolality
Osmotic forces
Aquaporins
Starling hypothesis

Net filtration = forces favoring filtration – forces
opposing filtration
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Water Movement Between
the ICF and ECF
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Net Filtration

Forces favoring filtration



Capillary hydrostatic pressure (blood pressure)
Interstitial oncotic pressure (water-pulling)
Forces favoring reabsorption


Plasma oncotic pressure (water-pulling)
Interstitial hydrostatic pressure
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Osmotic Equilibrium
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Alterations in Water Movement:
Edema


Accumulation of fluid within the interstitial
spaces
Causes




Increase in capillary hydrostatic pressure
Losses or diminished production of plasma albumin
Increases in capillary permeability
Lymph obstruction (lymphedema)
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Water Balance

Thirst perception

Osmolality receptors
• Hyperosmolality
 Baroreceptors stimulated
• Plasma volume depletion

ADH secretion
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Na+ and Cl– Balance

Sodium



Primary ECF cation
Regulates osmotic forces
Roles
• Neuromuscular irritability, acid-base balance, and cellular
reactions

Chloride


Primary ECF anion
Provides electroneutrality
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Na+ and Cl– Balance

Renin-angiotensin-aldosterone system


Aldosterone
Natriuretic peptides



Atrial natriuretic peptide
Brain natriuretic peptide
Urodilantin (kidney)
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Alterations in Na+, Cl–, and Water
Balance

Isotonic alterations

Total body water change with proportional
electrolyte change
 Isotonic volume depletion
 Isotonic volume excess
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Hypertonic Alterations

Hypernatremia

Serum sodium >147 mEq/L
 Related to sodium gain or water loss
 Water movement from the ICF to the ECF
• Intracellular dehydration
 Manifestations: intracellular dehydration,
convulsions, pulmonary edema, hypotension,
tachycardia
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Hypertonic Alterations

Water deficit

Dehydration
 Pure water deficits
 Renal free water clearance
 Manifestations
• Tachycardia, weak pulse, and postural hypotension
• Elevated hematocrit and serum sodium levels
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Hypertonic Alterations

Hyperchloremia

Occurs with hypernatremia or a bicarbonate deficit
 Usually secondary to pathophysiologic processes
 Managed by treating underlying disorders
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Hypotonic Alterations




Decreased osmolality
Hyponatremia or free water excess
Hyponatremia decreases the ECF osmotic
pressure, and water moves into the cell
Water movement causes symptoms related to
hypovolemia
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Hypotonic Alterations

Hyponatremia


Serum sodium level <135 mEq/L
Sodium deficits cause plasma hypoosmolality and
cellular swelling
• Pure sodium deficits
• Low intake
• Dilutional hyponatremia
• Hypoosmolar hyponatremia
• Hypertonic hyponatremia
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Hypotonic Alterations

Water excess



Compulsive water drinking
Decreased urine formation
Syndrome of inappropriate ADH (SIADH)
• ADH secretion in the absence of hypovolemia or
hyperosmolality
• Hyponatremia with hypervolemia

Manifestations: cerebral edema, muscle twitching,
headache, and weight gain
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Hypotonic Alterations

Hypochloremia



Usually the result of hyponatremia or elevated
bicarbonate concentration
Develops due to vomiting and the loss of HCl
Occurs in cystic fibrosis
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Potassium




Major intracellular cation
Concentration maintained by the Na+,K+
pump
Regulates intracellular electrical neutrality in
relation to Na+ and H+
Essential for transmission and conduction of
nerve impulses, normal cardiac rhythms, and
skeletal and smooth muscle contraction
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Potassium Levels

Changes in pH affect K+ balance


Hydrogen ions accumulate in the ICF during
states of acidosis. K+ shifts out to maintain a
balance of cations across the membrane.
Aldosterone, insulin, and catecholamines
influence serum potassium levels
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Hypokalemia




Potassium level <3.5 mEq/L
Potassium balance described by changes in
plasma potassium levels
Causes: reduced potassium intake, increased
potassium entry, and increased potassium
loss
Manifestations

Membrane hyperpolarization causes a decrease in
neuromuscular excitability, skeletal muscle
weakness, smooth muscle atony, and cardiac
dysrhythmias
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Hyperkalemia



Potassium level >5.5 mEq/L
Hyperkalemia is rare due to efficient renal
excretion
Caused by increased intake, shift of K+ from
ICF, decreased renal excretion, insulin
deficiency, or cell trauma
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Hyperkalemia

Mild attacks

Hypopolarized membrane, causing neuromuscular
irritability
• Tingling of lips and fingers, restlessness, intestinal
cramping, and diarrhea

Severe attacks

The cell is unable to repolarize, resulting in muscle
weakness, loss of muscle tone, flaccid paralysis,
cardiac arrest
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Calcium


Most calcium is located in the bone as
hydroxyapatite
Necessary for structure of bones and teeth,
blood clotting, hormone secretion, and cell
receptor function
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Phosphate



Like calcium, most phosphate (85%) is also
located in the bone
Necessary for high-energy bonds located in
creatine phosphate and ATP and acts as an anion
buffer
Calcium and phosphate concentrations are rigidly
controlled


Ca++ x HPO4– – = K+ (constant)
If concentration of one increases, that of the other
decreases
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Calcium and Phosphate

Regulated by three hormones


Parathyroid hormone (PTH)
• Increases plasma calcium levels via bone reabsorption
Vitamin D
• Fat-soluble steroid; increases calcium absorption from the GI
tract

Calcitonin
• Decreases plasma calcium levels
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Hypocalcemia and
Hypercalcemia

Hypocalcemia

Decreases the block
of Na+ into the cell
 Increased
neuromuscular
excitability
(partial
depolarization)
 Muscle cramps

Hypercalcemia

Increases the block
of Na+ into the cell
 Decreased
neuromuscular
excitability
 Muscle weakness
 Increased bone
fractures
 Kidney stones
 Constipation
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Hypophosphatemia and
Hyperphosphatemia

Hypophosphatemia






Osteomalacia
(soft bones)
Muscle weakness
Bleeding disorders
(platelet impairment)
Anemia
Leukocyte alterations
Antacids bind
phosphate

Hyperphosphatemia


See Hypocalcemia
High phosphate
levels are related to
the low calcium
levels
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Magnesium





Intracellular cation
Plasma concentration is 1.8 to 2.4 mEq/L
Acts as a co-factor in protein and nucleic acid
synthesis reactions
Required for ATPase activity
Decreases acetylcholine release at the
neuromuscular junction
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Hypomagnesemia and
Hypermagnesemia

Hypomagnesemia





Associated with
hypocalcemia and
hypokalemia
Neuromuscular
irritability
Tetany
Convulsions
Hyperactive reflexes

Hypermagnesemia






Skeletal muscle
depression
Muscle weakness
Hypotension
Respiratory
depression
Lethargy, drowsiness
Bradycardia
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pH: What Is It?

Negative logarithm of the H+ concentration
0
7
Increasing H+
Very acidic

pH scale
14
Decreasing H+
Neutral
Very alkaline
Each number represents a factor of 10. If a
solution moves from a pH of 7 to a pH of 6, the
H+ ions have increased 10-fold.
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pH





Inverse logarithm of the H+ concentration
H+ high in number, pH is low (acidic)
H+ low in number, pH is high (alkaline)
Ranges from 0 to 14
Each number represents a factor of 10.

If a solution moves from a pH of 6 to a pH of 5, the
H+ has increased 10 times
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pH



Acids are formed as end products of protein,
carbohydrate, and fat metabolism
To maintain the body’s normal pH (7.35-7.45)
the H+ must be neutralized or excreted
Bones, lungs, and kidneys are major organs
involved in regulation of acid-base balance
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pH

Body acids exist in two forms


Volatile
• H2CO3 (can be eliminated as CO2 gas)
Nonvolatile
• Sulfuric, phosphoric, and other organic acids
• Eliminated by the renal tubules with the regulation of
HCO3–
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Buffering Systems

Buffer systems exist as buffer pairs


Associate and dissociate very quickly
(instantaneous)
Buffer changes occur in response to changes in
acid-base status
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Buffering Systems



A buffer is a chemical that can bind excessive
H+ or OH– without a significant change in pH
A buffering pair consists of a weak acid and
its conjugate base
The most important plasma buffering systems
are the carbonic acid–bicarbonate system
and hemoglobin
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Carbonic Acid–Bicarbonate Pair


Operates in the lung and the kidney
The greater the partial pressure of carbon
dioxide, the more carbonic acid is formed


At a pH of 7.4, the ratio of bicarbonate to carbonic
acid is 20:1
Bicarbonate and carbonic acid can increase or
decrease, but the ratio must be maintained
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Carbonic Acid–Bicarbonate Pair


If amount of bicarbonate decreases, the pH
decreases, causing a state of acidosis
The pH can be returned to normal if the
amount of carbonic acid also decreases



This type of pH adjustment is called compensation
The respiratory system compensates by increasing or
decreasing ventilation
The renal system compensates by producing acidic
or alkaline urine
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Other Buffering Systems

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–
Cellular ion exchange
 Exchange of K+ for H+ in acidosis and alkalosis
(alters serum potassium)
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Acid-Base Imbalances

Normal arterial blood pH



Acidosis


7.35 to 7.45
Obtained by arterial blood gas (ABG) sampling
Systemic increase in H+ concentration
Alkalosis

Systemic decrease in H+ concentration
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Acidosis and Alkalosis

Four categories of acid-base imbalances




Respiratory acidosis—elevation of pCO2 due to
ventilation depression
Respiratory alkalosis—depression of pCO2 due to
alveolar hyperventilation
Metabolic acidosis—depression of HCO3– or an
increase in noncarbonic acids
Metabolic alkalosis—elevation of HCO3– usually due to
an excessive loss of metabolic acids
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Compensation

Renal


Alters bicarbonate and H+ levels in response to
acidosis or alkalosis
• Much slower response
• Excretion and/or reabsorption
Respiratory

Alters CO2 retention or loss in response to
alkalosis or acidosis
• Rapid response
• Respiratory rate alterations
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Compensation

When adjustments are made to bicarbonate
and carbonic acid in order to maintain the
20:1 ratio and therefore maintain normal pH

The actual values for bicarbonate to carbonic acid
ratio are not normal but the normal ratio is
achieved
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Correction

Correction occurs when the values for BOTH
components of the buffer pair (carbonic acid and
bicarbonate) have also returned to normal levels
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Metabolic Acidosis
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Anion Gap



Used cautiously to distinguish different types
of metabolic acidosis
By rule, the concentration of anions (–)
should equal the concentration of cations (+).
Not all normal anions are routinely measured.
Normal anion gap =
Na+ + K+ = Cl– + HCO3– + 10 to 12 mEq/L
(other misc. anions [the ones we don’t
measure]—phosphates, sulfates, organic
acids, etc.)
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Anion Gap

Abnormal anion gap occurs due to an
increased level of abnormal unmeasured
anion


Examples: DKA—ketones, salicylate poisoning,
lactic acidosis—increased lactic acid, renal failure,
etc.
As these abnormal anions accumulate, the
measured anions have to decrease to
maintain electroneutrality
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Metabolic Alkalosis
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Respiratory Acidosis
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Respiratory Alkalosis
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Summary
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