1 The Cellular Environment: Fluids and Electrolytes, Acids and Bases Chapter 3.

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The Cellular Environment: Fluids and Electrolytes, Acids and BasesChapter 3

Mosby items and derived items © 2006 by Mosby, Inc.

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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

1 The Cellular Environment: Fluids and Electrolytes, Acids and Bases Chapter 3.

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mosby items

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water balance slide

movement of water

water loss water movement

water excess compulsive

ecf slide

edema slide