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1
The Cellular Environment: Fluids and Electrolytes, Acids and BasesChapter 3
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Distribution of Body Fluids Total body water (TBW) 60% of total body
weight Intracellular fluid – inside the cells Extracellular fluid – not encased in cells
Interstitial fluid – found in between cells and tissues
Intravascular fluid- plasma found in circulatory system
Lymph, synovial, intestinal, biliary, hepatic, pancreatic, CSF, sweat, urine, pleural, peritoneal, pericardial, and intraocular fluids are extracellular
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Water Movement Between the ICF and ECF Osmolality – the concentrations of solutes in water Osmotic forces – solutes will influence the
movement of water across membranes Aquaporins- water channel proteins in membranes Starling hypothesis
Net filtration = forces favoring filtration – forces opposing filtration
As fluid flows through capillary it looses water and create greater osmotic return of water as it flows toward veinule end of capillary
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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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Edema
Accumulation of fluid within the interstitial spaces
Causes: Increase in hydrostatic pressure Losses or diminished production of plasma
albumin Increases in capillary permeability Lymph obstruction – elephantitus, flibitus
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Edema
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Water Balance
Thirst perception Osmolality receptors in medula respond to
osmotic pressue of ECF Hyperosmolality and plasma volume depletion
ADH secretion from posterior pituitary – conserves water in kidney to maintain water balance
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Sodium and Chloride 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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Sodium and Chloride Balance
Renin-angiotensin system – substanced produced in both liver and kidney
Angiotensin produced by liver and coverted by enzymes activated by renin from Kidney Juxta Glomerular Aparatus to a powerful vasoconstrictor. Aldosterone – hormone from adrenal gland to regulate Na and K
Natriuretic peptides Atrial natriuretic peptide - hormone from heart Brain natriuretic peptide – hormone from brain Urodilantin (kidney) – Kidney hormone
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Alterations in Na+, Cl–, and Water Balance
Isotonic alterations Total body water change with proportional
electrolyte and water 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, etc.
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Water Deficit
Dehydration Pure water deficits Renal free water clearance Manifestations
Tachycardia, weak pulses, and postural hypotension
Elevated hematocrit and serum sodium level
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Hypochloremia
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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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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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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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 is described by changes in plasma
potassium levels Causes can be reduced intake of potassium,
increased entry of potassium, and increased loss of potassium
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 not able to repolarize, resulting in
muscle weakness, loss or muscle tone, and flaccid paralysis
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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 the 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
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 cofactor 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 Inverse logarithm of the H+ concentration If the H+ are high in number, the pH is low
(acidic). If the H+ are low in number, the pH is high (alkaline).
The pH scale ranges from 0 to 14: 0 is very acidic, 14 is very alkaline. Each number represents a factor of 10. If a solution moves from a pH of 6 to a pH of 5, the H+ have 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 The bones, lungs, and kidneys are the major
organs involved in the regulation of acid and 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 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 both 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 the 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 referred to as compensation
The respiratory system compensates by increasing or decreasing ventilation
The renal system compensates by producing acidic or alkaline urine
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Carbonic Acid–Bicarbonate Pair
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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
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Buffering Systems
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Acid-Base Imbalances Normal arterial blood pH
7.35 to 7.45 Obtained by arterial blood gas (ABG) sampling
Acidosis 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 non-carbonic acids Metabolic alkalosis—elevation of HCO3
– usually due to an excessive loss of metabolic acids
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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 An abnormal anion gap occurs due to an
increased level of an 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