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The Nature of Disease
Pathology for the Health Professions
Thomas H. McConnell
Chapter 6
Alterations of Fluid, Electrolyte,
Acid-Base Balance
Lecture 6, Part 1
Overview of Today’s Lecture
– Fluid Imbalance
– Electrolyte imbalance
– Acid-base balance/imbalance
– Acidosis and alkalosis
Overview
• Our survival depends upon maintaining a
normal volume and composition of
– Extracellular fluid (ECF)
– Intracellular fluid (ICF)
• Ionic concentrations and pH are critical
• Three interrelated processes
– Fluid balance (How does water move from one place to the other? )
– Electrolyte balance (What is an electrolyte?)
– Acid-base balance (What is normal pH?)
3
Osmolarity and Milliequivalents (mEq)
• Recall that osmolarity expresses total solute
concentration of a solution
– Osmolarity (effect on H2O) of body solutions is determined
by the total number of dissolved particles (regardless of
where they came from)
– The term ‘osmole’ reflects the number of particles yielded
by a particular solute (milliosmole, mOsm, = osmole/1000)
• 1 mole of glucose (180g/mol) -> 1 osmole of particles
• 1 mole of NaCl (58g/mol) -> 2 osmoles of particles
• Osmolarity = #moles/L X # particles yielded
• An equivalent is the positive or negative charge equal
to the amount of charge in one mole of H+
– A milliequivalent (mEq) is one-thousandth of an Eq
– Number of Eq = #moles/L X valence
4
Osmolarity
The human body has:
- an osmolarity of 275 – 300 mOsm/L
- about 40 L of H2O
Amount of solute (osmoles)
Osmolarity (osm/L) =
Volume of H2O (liters)
Approximately how many total osmoles of solute are
there in the human body?
How can you change the osmolarity of a body fluid?
5
Tonicity
(1)
H2O
(1)
H2O
Hypertonic
Blood
Hypotonic
Blood
(3)
(2)
(2)
H2O
H2O
H2O
H2O
(3)
H2O
H2O
Fluid Compartments
Figure from: Hole’s Human A&P, 12th edition, 2010
Major ions of ICF: K+, Mg2+, PO43-
Major ions of ECF:
Na+, Cl-, HCO3‘Compartments’ commonly behave as distinct entities in terms of
ion distribution, but ICF and ECF osmotic pressures are identical
(about 290-300 mOsm/L) in both compartments. Why?
7
Water Content of the Human Body
Approximate percent body water:
- Adult male: 60%
- Adult female: 50%
- Infants: 75-80%
- Geriatric: 45%
Of the 40 liters of water in the body
of an average adult male:
- one-third (15L) is extracellular
- two-thirds (25L) is intracellular
Figure from: Hole’s Human A&P, 12th edition, 2010
8
Movement of Fluids Between Compartments
Figure from: Hole’s Human A&P, 12th edition, 2010
Third spacing:
accumulation/trapping
of fluid in areas where
it’s unavailable for
metabolic processes or
perfusion.
Water moves between
mesothelial surfaces:
peritoneal, pleural, and
pericardial cavities as well
as the synovial
membranes. It also moves
between the blood and
CSF and through the fluids
of the eye and ear
Net movements of fluids between compartments result from differences in
hydrostatic and osmotic pressures (Starling’s forces)
9
Fluid (Water) Balance
Figure from: Hole’s Human A&P, 12th edition, 2010
* urine production is the most important regulator of water
balance (water in = water out)
10
Water Balance and ECF Osmolarity
• Regulation of water intake
• increase in osmotic pressure of ECF → osmoreceptors in
hypothalamic thirst center → stimulates thirst and drinking
(water! )
• Regulation of water output
• Obligatory water losses (must happen)
• insensible water losses (lungs, skin)
• water loss in feces
• water loss in urine (min about 500 ml/day)
• increase in osmotic pressure of ECF → ADH is released
• concentrated urine is excreted
• more water is retained
• LARGE changes in blood vol/pressure → Renin and ADH
release
11
Edema
Accumulation of fluid within the interstitial spaces
Figure from: Huether & McCance,
Understanding Pathology, 5th ed.,
Elsevier, 2012
Figure from: McConnell,
The Nature of Disease, 2nd
ed., LWW, 2014
• Localized vs. generalized (anasarca)
• Pitting edema (low protein, transudate)
• Non-pitting edemas (inflammatory or lymphedema,
exudate)
Fluid Imbalance
Figure from: Saladin, Anatomy & Physiology, McGraw Hill, 2007
13
Dehydration and Overhydration
Dehydration (removing only H2O)
• osmotic pressure increases
in extracellular fluids
• water moves out of cells
• osmoreceptors in
hypothalamus stimulated
• hypothalamus signals
posterior pituitary to release
ADH
• urine output decreases
Severe thirst, wrinkling of skin
(decreased turgor), fall in plasma
volume and decreased blood
pressure, circulatory shock, death
Overhydration (adding only H2O)
• osmotic pressure decreases
in extracellular fluids
• water moves into cells
• osmoreceptors inhibited in
hypothalamus
• hypothalamus signals
posterior pituitary to decrease
ADH output
• urine output increases
‘Drunken’ behavior (water
intoxication), confusion,
hallucinations, convulsions, coma,
death
Severity of dehydration categorized by relative amount of lost body weight:
2% = mild, 5% moderate, 8% = severe
14
Electrolyte Balance
Electrolyte balance is important
since:
Figure from: Hole’s Human A&P, 12th edition, 2010
1. It regulates fluid (water)
balance
2. Concentrations of
individual electrolytes can
affect cellular functions
Remember that:
- water follows solute
- Cl- follows Na+
Na+plasma: 136-142 mEq/L; Avg ≈ 140
K+: plasma: 3.8-5.0 mEq/L; Avg ≈ 4.0
15
Hyper- and Hyponatremia
Figures from: Martini, Anatomy
& Physiology, Prentice Hall,
2001
Hypernatremia > 147 mEq/L Na+
Osmolarity is
regulated by
altering H2O
content
** Osmolarity = Amt of solute / volume of H2O
Hyponatremia < 135 mEq/L Na+
16
Fluid Volume Regulation and [Na+]
Volume is
regulated by
altering Na+
content
Figures from: Martini,
Anatomy & Physiology,
Prentice Hall, 2001
Estrogens are
chemically similar to
aldosterone and enhance
NaCl absorption by
renal tubules
Glucocorticoids can
also enhance tubular
reabsorption of Na+
17
Summary Table of Fluid and Electrolyte Balance
Condition
Initial Change
 H2O in the ECF
Change in
OSMOLARITY
(**Corrected by change
in H2O levels)
 H2O in the ECF
 H2O/Na+ in the ECF
Initial Effect
Correction
 Na+ concentration,
 Thirst →  H2O intake
 ECF osmolarity
 ADH →  H2O output
 Na+ concentration,
 Thirst →  H2O intake
 ECF osmolarity
 ADH →  H2O output
 volume,
 BP
Change in VOLUME
(**Corrected by change
in Na+ levels)
 H2O/Na+ in the ECF
 volume,
 BP
Renin-angiotensin:
 Thirst
 ADH
 aldosterone
 vasoconstriction
Natriuretic peptides:
 Thirst
 ADH
 aldosterone
You should understand this table
Result
 H2O in the ECF
 H2O in the ECF
 H2O intake
 Na+/H2O reabsorption
 H2O loss
 H2O intake
 Na+/H2O reabsorption
 H2O loss
18
Sodium Imbalance
• Hyponatremia (low [Na+]; < 135 mEq/L)
• Causes
• Excessive loss, e.g., sweating, vomiting, diarrhea
• Excessive water ingestion
• Some diruretics
• Effects
• Impaired nerve transmission
• H2O shift into cells
• Intracellular edema, esp. in brain cells
• Muscle cramps
19
Sodium Imbalance
• Hypernatremia (high [Na+]; > 145 mEq/L)
• Causes
• Excessive Na+ ingestion
• Dehydration
• Decreased ADH action (rare)
• Effects
• Increased osmotic pressure of plasma
• H2O shifts out of cells
• Weakness, agitation
• Decreased urine output
20
Potassium Balance
Figure from: Hole’s Human A&P, 12th edition, 2010
Potassium loss generally
occurs via the urine.
The rate of tubular
secretion of K+ varies
with:
1. Changes in the [K+] in
the ECF
2. Changes in pH
3. Aldosterone levels
Remember that Na+ can be
exchanged for H+ or K+ in
the nephron tubules
21
Potassium Imbalance
• Hypokalemia (Low potassium; < 3.5 mEq/L)
- Causes
- Fecal loss with diarrhea
- Low dietary intake
- Drugs, e.g., diuretics
- High aldosterone/cortisol levels
- High doses of insulin
-Effects
- Arrythmias
- Skeletal muscle weakness
- Paresthesias (tingling nerves)
• Hyperkalemia (High potassium; > 5.0 mEq/L)
- Causes
- Renal failure
- Drugs, e.g., antihypertensive
-Effects
- Interference with neuron transmission
-Muscle weakness
-High levels cause cardiac arrest
Figure from: Huether & McCance,
Understanding Pathology, 5th ed.,
Elsevier, 2012
Calcium & Phosphate Balance
Figure from: Hole’s Human A&P, 12th edition, 2010
[Ca2+] in ECF is about
5 mEq/L
Calcium and phosphate
concentrations are rigidly
controlled, and are inversely
related:
Ca2+ x HPO43– = constant
23
Hypocalcemia
• Relatively uncommon; < 4.25 mEq/L
• 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
• Tingling, muscle spasm (particularly in hands, feet, and facial muscles),
intestinal cramping, hyperactive bowel sounds
– Severe cases show convulsions and tetany
– Prolonged QT interval, cardiac arrest
– Bone pain, osteoporosis
Hypercalcemia
• Much more common than hypocalcemia; > 5.25 mEq/L
• Causes
– Hyperparathyroidism
– Bone metastases with calcium resorption from breast,
prostate, renal, and cervical cancer
– Sarcoidosis
– Excess vitamin D
– Many tumors that produce PTH
• Effects:
– Many nonspecific: fatigue, weakness, lethargy, anorexia,
nausea, constipation
– Impaired renal function, kidney stones
– Dysrhythmias, bradycardia, cardiac arrest
Phosphate
• Most phosphate is located in the bone (like calcium)
• Necessary for high-energy bonds located in creatine phosphate
and ATP and acts as an anion buffer
• Hypophosphatemia (low blood phosphate)
– Diarrhea
– Any condition that raises blood calcium
• Hyerphosphatemia (high blood calcium)
– Renal failure (most common cause)
• Sequellae of phosphate abnormalities closely coupled to those
of calcium previously discussed.
Magnesium
• Intracellular cation
• Acts as a cofactor in intracellular enzymatic reactions
• Hypomagnesemia (low blood magnesium)
– Dietary deficiency, usually
– Effects usually related to hypocalcemia/hypokalemia
• Lethargy, tremor, tetany, arrhythmias, and seizures
• Hypermagnesemia (high blood magnesium)
– Renal failure is typical cause
– Effects
• Hypotension, depressed respiration, arryhthmias or cardiac
arrest
Hydrogen Ions and Acids
Figure from: Hole’s Human A&P, 12th edition, 2010
Some H+ is also absorbed from the digestive tract
Classification of acids:
- Volatile, e.g., CO2; leave solution and enter atmosphere
- Fixed acids; non-volatile and include
- ingested amino acids (meat)
- ketones produced from fatty acid metabolism
28
Regulation of Hydrogen Ion Concentration
1. chemical acid-base buffer systems (physical buffers)
• first line of defense
• can tie-up acids or bases, but cannot eliminate them
• act in seconds
2. respiratory excretion of carbon dioxide
• a physiological buffer (can eliminate excess acid indirectly
via CO2)
• minutes
3. renal excretion of hydrogen ions
• a physiological buffer (can eliminate excess metabolic acids
directly, e.g., keto-, uric, lactic, phosphoric)
• hours to a day
29
Acid-Base Buffer Systems
Bicarbonate System
• the bicarbonate ion converts a strong acid to a weak acid
• carbonic acid converts a strong base to a weak base
• an important buffer of the ECF (plasma [HCO3-] ~ 25 mEq/L)
H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O
**At pH 7.4: [HCO3-] / [H2CO3] = 20:1
Phosphate System
• the monohydrogen phosphate ion converts a strong acid to a
weak acid
• the dihydrogen phosphate ion converts a strong base to a
weak base
Strong acid
Weak acid
H+ + HPO4-2 ↔ H2PO430
Acid-Base Buffer Systems
Protein Buffer System
ICF, plasma proteins, Hb
COOH group
releases
hydrogen ions
when pH rises
Most plentiful and powerful
chemical buffer system
NH2 group
accepts
hydrogen ions
when pH falls
-
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001
31
Respiratory Excretion of Carbon Dioxide
Figure from: Hole’s Human A&P, 12th edition, 2010
A physiological
buffer system
32
Renal Excretion of Hydrogen Ions
Figure from: Hole’s Human A&P, 12th edition, 2010
*The kidney is most powerful and
versatile acid-base regulating system
in the body
33
Buffering Mechanisms in the Kidney
Note that secretion of H+
relies on carbonic
anhydrase activity within
tubular cells
Net result is secretion of
H+ accompanied by the
(1)retention of HCO3(2)
Figure from: Martini,
Anatomy &
Physiology, Prentice
Hall, 2001
Production of
new HCO3-
34
Summary of Acid-Base Balance
Figure from: Hole’s Human A&P, 12th edition, 2010
(Seconds)
Know this slide!
(Minutes)
(Hours-Days)
35
Acidosis and Alkalosis
If the pH of arterial blood drops to 6.8 or rises to 8.0 for more than a few
hours, survival is jeopardized
Classified according to:
1. Whether the cause is
respiratory (CO2), or
metabolic (other
acids, bases)
2. Whether the blood
pH is acid or alkaline
Figure from: Hole’s Human A&P, 12th edition, 2010
36
Acidosis
Figure from: Hole’s Human A&P, 12th edition, 2010
(hypopnea)
Respiratory acidosis
Metabolic acidosis
Nervous system depression, coma, death
37
Alkalosis
Figure from: Hole’s Human A&P, 12th edition, 2010
Respiratory alkalosis
Metabolic alkalosis
Nervousness, tetany, convulsions, death
38
Table from: McConnell, The Nature of Disease, 2nd ed., LWW, 2014
39
Figure from: McConnell, The Nature of Disease, 2nd ed., LWW, 2014
40
Acidosis and Alkalosis
• What would be the indications of acidosis
and alkalosis in terms of changes in pH and
PCO2? pH and HCO3-?
• How would the body try to compensate for
– Acidosis (↓pH)
• Respiratory (↑pCO2)
• Metabolic (↓HCO3-)
– Alkalosis (↑ pH)
• Respiratory (↓pCO2)
• Metabolic (↑HCO3-)
41
Flow chart for Acidosis/Alkalosis
Three things to check:
1) pH – 7.35-7.45
2) pCO2 – 35-45 mm Hg
3) HCO3- - 22 – 26 mEq/L
pH


acidosis
 pCO2
respiratory
Norm
HCO3-
HCO3-
alkalosis
 HCO3metabolic
Norm
pCO2
No Comp
No Comp
Comp
 pCO2
HCO3-
respiratory
 pCO2
Comp
Norm
HCO3-
 HCO3-
No Comp
Comp
metabolic
Norm
pCO2
No Comp
 pCO2
Comp
42