Chapter 27

Fluid, Electrolyte and Acid-Base Homeostasis

Body fluid
all the water and dissolved solutes in the bodys fluid compartments

Mechanisms regulate
total volume distribution concentration of solutes and pH

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Balance Between Fluid Compartments

Volume of fluid in each is kept constant. Since water follows electrolytes, they must be in balance as well

Only 2 places for exchange between compartments:

cell membranes separate intracellular from interstitial fluid. only in capillaries are walls thin enough for exchange between plasma and 9/e 2000 JWS Tortora & Grabowski interstitial fluids 27-2

Body Water Gain and Loss

45-75% body weight
declines with age since fat contains almost no water

Gain from ingestion and metabolic water formed during aerobic respiration & dehydration synthesis reactions (2500 mL/day) Normally loss = gain
urine, feces, sweat, breathe
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Regulation of Water Gain

Formation of metabolic water is not regulated
function of the need for ATP

Main regulator of water gain is intake regulation Stimulators of thirst center in hypothalamus
dry mouth, osmoreceptors in hypothalamus, decreased blood volume causes drop in BP & angiotensin II

Drinking occurs
body water levels return to normal
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Dehydration Stimulates Thirst

Regulation of fluid gain is by regulation of thirst.

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Regulation of Water and Solute Loss

Elimination of excess water or solutes occurs through urination Consumption of very salty meal demonstrates function of three hormones Demonstrates how
water follows salt excrete Na+ and water will follow and decrease blood volume
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Hormone Effects on Solutes

Angiotensin II and aldosterone promote reabsorption of Na+ and Cl- and an increase in fluid volume
stretches atrial volume and promotes release of ANP slows release of renin & formation of angiotensin II
increases filtration rate & reduces water & Na+ reabsorption decreases secretion of aldosterone slowing reabsorption of Na+ and Cl- in collecting ducts

ANP promotes natriuresis or the increased excretion of Na+ and Cl- which decreases blood volume
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Hormone Regulation of Water Balance

Antidiuretic hormone (ADH) from the posterior pituitary
stimulates thirst increases permeability of principal cells of collecting ducts to assist in water reabsorption very concentrated urine is formed

ADH secretion shuts off after the intake of water ADH secretion is increased
large decrease in blood volume severe dehydration and drop in blood pressure vomiting, diarrhea, heavy sweating or burns
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Movement of Water
Intracellular and interstitial fluids normally have the same osmolarity, so cells neither swell nor shrink Swollen cells of water intoxication because Na+ concentration of plasma falls below normal
drink plain water faster than kidneys can excrete it replace water lost from diarrhea or vomiting with plain water may cause convulsions, coma & death unless oral rehydration includes small amount salt in water intake
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Enemas and Fluid Balance

Introduction of a solution into the bowel to stimulate activity and evacuate feces Increase risk of fluid & electrolyte imbalance unless isotonic solution is used

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Concentrations of Electrolytes
Functions of electrolytes
control osmosis between fluid compartments help maintain acid-base balance carry electric current cofactors needed for enzymatic activity

Concentration expressed in mEq/liter or milliequivalents per liter for plasma, interstitial fluid and intracellular fluid
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Comparison Between Fluid Components

Plasma contains many proteins, but interstitial fluid does not

producing blood colloid osmotic pressure

Extracellular fluid contains Na+ and Cl Intracellular fluid contains K+ and phosphates (HPO4 -2)
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Sodium
Most abundant extracellular ion
accounts for 1/2 of osmolarity of ECF

Average daily intake exceeds normal requirements Hormonal controls

aldosterone causes increased reabsorption Na+ ADH release ceases if Na+ levels too low--dilute urine lost until Na+ levels rise ANP increases Na+ and water excretion if Na+ levels too high
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Edema, Hypovolemia and Na+ Imbalance

Sodium retention causes water retention
edema is abnormal accumulation of interstitial fluid

Causes of sodium retention

renal failure hyperaldosterone

Excessive loss of sodium causes excessive loss of water (low blood volume)
due to inadequate secretion of aldosterone too many diuretics
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Chloride
Most prevalent extracellular anion Moves easily between compartments due to Clleakage channels Helps balance anions in different compartments Regulation
passively follows Na+ so it is regulated indirectly by aldosterone levels ADH helps regulate Cl- in body fluids because it controls water loss in urine

Chloride shift & hydrochloric acid of gastric juice

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Potassium
Most abundant cation in intracellular fluid Helps establish resting membrane potential & repolarize nerve & muscle tissue Exchanged for H+ to help regulate pH in intracellular fluid Control is mainly by aldosterone which stimulates principal cells to increase K+ secretion into the urine
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abnormal plasma K+ levels adversely affect cardiac and neuromuscular function

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Bicarbonate
Common extracellular anion Major buffer in plasma Concentration increases as blood flows through systemic capillaries due to CO2 released from metabolically active cells Concentration decreases as blood flows through pulmonary capillaries and CO2 is exhaled Kidneys are main regulator of plasma levels
intercalated cells form more if levels are too low excrete excess in the urine
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Calcium
Most abundant mineral in body (skeleton & teeth) Abundant extracellular cation in body fluids Important role in blood clotting, neurotransmitter release, muscle tone & nerve and muscle function Regulated by parathyroid hormone
stimulates osteoclasts to release calcium from bone increases production of calcitriol (Ca+2 absorption from GI tract and reabsorption from glomerular filtrate) Tortora & Grabowski 9/e 2000 JWS 27-18

Phosphate
Present as calcium phosphate in bones and teeth, and in phospholipids, ATP, DNA and RNA HPO4 -2 is important intracellular anion and acts as buffer of H+ in body fluids and in urine
mono and dihydrogen phosphate act as buffers in the blood

Plasma levels are regulated by parathyroid hormone & calcitriol

resorption of bone releases phosphate in the kidney, PTH increase phosphate excretion calcitriol increases GI absorption of phosphate
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Magnesium
Found in bone matrix and as ions in body fluids
intracellular cofactor for metabolic enzymes, heart, muscle & nerve function

Urinary excretion increased in hypercalcemia, hypermagnesemia, increased extracellular fluid volume, decreases in parathyroid hormone and acidosis

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Acid-Base Balance
Homeostasis of H+ concentration is vital
proteins 3-D structure sensitive to pH changes normal plasma pH must be maintained between 7.35 - 7.45 diet high in proteins tends to acidify the blood

3 major mechanisms to regulate pH

buffer system exhalation of CO2 (respiratory system) kidney excretion of H+ (urinary system)
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Actions of Buffer Systems

Prevent rapid, drastic changes in pH Change either strong acid or base into weaker one Work in fractions of a second Found in fluids of the body 3 principal buffer systems
protein buffer system carbonic acid-bicarbonate buffer system phosphate buffer system
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Protein Buffer System

Abundant in intracellular fluids & in plasma
hemoglobin very good at buffering H+ in RBCs albumin is main plasma protein buffer

Amino acids contains at least one carboxyl group (-COOH) and at least one amino group (-NH2)
carboxyl group acts like an acid & releases H+ amino group acts like a base & combines with H+ some side chains can buffer H+

Hemoglobin acts as a buffer in blood by picking up CO2 or H+

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Carbonic Acid-Bicarbonate Buffer System

Acts as extracellular & intracellular buffer system
bicarbonate ion (HCO3-) can act as a weak base
holds excess H+

carbonic acid (H2CO3) can act as weak acid

dissociates into H+ ions

At a pH of 7.4, bicarbonate ion concentration is about 20 times that of carbonic acid Can not protect against pH changes due to respiratory problems
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Phosphate Buffer System

Most important intracellularly, but also acts to buffer acids in the urine Dihydrogen phosphate ion acts as a weak acid that can buffer a strong base Monohydrogen phosphate acts a weak base by buffering the H+ released by a strong acid
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Exhalation of Carbon Dioxide

Breathing plays a role in the homeostasis of pH pH modified by changing rate & depth of breathing
faster breathing rate, blood pH rises slow breathing rate, blood pH drops

H+ detected by chemoreceptors in medulla oblongata, carotid & aortic bodies Respiratory centers inhibited or stimulated by 2000 JWS is pH changes Tortora & Grabowski 9/e

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Kidney Excretion of H+
Metabolic reactions produce 1mEq/liter of nonvolatile acid for every kilogram of body weight Excretion of H+ in the urine is only way to eliminate huge excess Kidneys synthesize new bicarbonate and save filtered bicarbonate Renal failure can cause death rapidly due to its role in pH balance
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Acid-Base Imbalances
Acidosis---blood pH below 7.35 Alkalosis---blood pH above 7.45 Compensation is an attempt to correct the problem
respiratory compensation renal compensation

Acidosis causes depression of CNS---coma Alkalosis causes excitability of nervous tissue---spasms, convulsions & death
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Summary of Causes
Respiratory acidosis & alkalosis are disorders involving changes in partial pressure of CO2 in blood Metabolic acidosis & alkalosis are disorders due to changes in bicarbonate ion concentration in blood

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Respiratory Acidosis
Cause is elevation of pCO2 of blood Due to lack of removal of CO2 from blood
emphysema, pulmonary edema, injury to the brainstem & respiratory centers

Treatment
IV administration of bicarbonate (HCO3-) ventilation therapy to increase exhalation of CO2
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Respiratory Alkalosis
Arterial blood pCO2 is too low Hyperventilation caused by high altitude, pulmonary disease, stroke, anxiety, aspirin overdose Renal compensation involves decrease in excretion of H+ and increase reabsorption of bicarbonate Treatment
breathe into a paper bag
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Metabolic Acidosis
Blood bicarbonate ion concentration too low
loss of ion through diarrhea or kidney dysfunction accumulation of acid (ketosis with dieting/diabetes) kidney failing to remove H+ from protein metabolism

Respiratory compensation by hyperventilation Treatment

IV administration of sodium bicarbonate correct the cause
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Metabolic Alkalosis
Blood bicarbonate levels are too high Cause is nonrespiratory loss of acid
vomiting, gastric suctioning, use of diuretics, dehydration, excessive intake of alkaline drugs

Respiratory compensation is hypoventilation Treatment

fluid and electrolyte therapy correct the cause
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Diagnosis of Acid-Base Imbalances

Evaluate
systemic arterial blood pH concentration of bicarbonate (too low or too high) PCO2 (too low or too high)

Solutions
if problem is respiratory, the pCO2 will not be normal if problem is metabolic, the bicarbonate level will not be normal
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Homeostasis in Infants
More body water in ECF so more easily disrupted Rate of fluid intake/output is 7X higher Higher metabolic rate produces more metabolic wastes Kidneys can not concentrate urine nor remove excess H+ Surface area to volume ratio is greater so lose more water through skin Higher breathing rate increase water loss from lungs Higher K+ and Cl- concentrations than adults

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Impaired Homeostasis in the Elderly

Decreased volume of intracellular fluid
inadequate fluid intake

Decreased total body K+ due to loss of muscle tissue or potassium-depleting diuretics for treatment of hypertension or heart disease Decreased respiratory & renal function
slowing of exhalation of CO2 decreased blood flow & glomerular filtration rate reduced sensitivity to ADH & impaired ability to produce dilute urine renal tubule cells produce less ammonia to combine with H+ and excrete as NH+4
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