Chapter 27

Chapter 27Fluid, Electrolyte,

and Acid-Base Homeostasis

Copyright © John Wiley & Sons, Inc. All rights reserved.

The fluid compartments of the body are all

contained in either the intracellular compartment

or the extracellular compartment

Intracellular fluid is all fluid contained inside

cells, and comprises 2/3 of all body fluids

Extracellular fluid is all fluid outside the cells.

1/3 of all body fluid is contained in the

extracellular compartment

Fluid Compartments


Intracellular fluid (ICF) – about two thirds by volume

Extracellular fluid (ECF) – consists of: Plasma Interstitial fluid (IF) – fluid in tissue spaces Other ECF – lymph, CSF, synovial fluid,

serous fluid etc.

Fluid Compartments


Babies are more “wet”

than adults, with water

composing about 80%

of total body mass

Fluid Compartments

Water makes up 55–80% of total body mass (depending on age and sex)


Extracellular fluids (ECFs) are similar (except for

the high protein content of plasma)

Sodium is the chief cation, chloride is the major anion

Intracellular fluid

Potassium is the chief cation, phosphate is the chief

anion

Three times protein content than plasma

Sodium and potassium concentrations in ECF & ICF are

opposite due:

Cell membrane Na+/ K+ ATPase pump

Composition of Body Fluids


Exchange occurs across capillary membranes

At the arterial end, net HP is more (fluid flows out)

At the venous end of a bed, net COP is more ( fluid flows in)

Any leakage of fluid from the blood is picked up by lymphatics & returned to the blood

Fluid movement between plasma & interstitial fluid

HP 35

HP16


Exchanges between IF & ICF occur across

plasma membrane- depend on membrane

permeability

Water moves according to osmotic

gradients; from low osmolarity to high

osmolarity (from more water to less

water)

Fluid movement between intracellular fluid & interstitial fluid


Fluid movement between compartments:Fluid movement after fluid intake: when you drink water, water enters your blood from the digestive system plasma osmolarity decreasesWater moves out of plasma to become part of the interstitial fluid, and then moves from the interstitial fluid into cells Reverse when dehydrated


Normal fluid intake is through:

Ingestion of liquids and moist foods (2300mL/day)

Metabolic synthesis of water during cellular

respiration and dehydration synthesis (200mL/day)

Normal fluid loss is through:

The kidneys (1500mL/day)

Evaporation from the skin (600mL/day)

Exhalation from the lungs (300mL/day)

In the feces (100mL/day)

Fluid Balance


Fluid intake and output (I & O) are usually

balanced on a daily basis, despite the fact that

intake of water and electrolytes

are rarely proportional

The kidneys excrete

excess water through

dilute urine, or retain water

through concentrated urine

Fluid Balance


The hypothalamic thirst center is stimulated:

By increases in plasma osmolarity- even a small increase (by stimulating osmoreceptors in the hypothalamus)

thirst increases water intake – osmolarity becomes normal

decreased salivary secretions- sensory input relayed from receptors in mucous membranes to thirst center

decreased blood pressure (significant decrease)

◦ renin released from kidney- in response angiotensin II is

formed which stimulates the thirst center

Regulation of water intake- the thirst mechanism


Fluid Intake


Antidiuretic hormone (ADH) plays a major role in

directly regulating water loss in the collecting ducts of

the kidneys Rise in osmolarity stimulates hypothalamic

osmoreceptors -triggers ADH release Significant decrease in blood volume/BP also triggers

ADH release, but rise in osmolarity more potent stimulus

ADH increases permeability of the collecting ducts to

water by insertion of aquaporins into the principal

cells – water reabsorbed-producing a concentrated

small volume urine- water retained in the body

When ADH levels low- water in CDs not reabsorbed-

producing dilute urine

Regulation of Water Output


Mechanisms and Consequences of

ADH Release


Water output also regulated by:

Aldosterone: promotes urinary Na+ reabsorption

(followed by water by osmosis) & decrease urine

output

Atrial natriuretic peptide (ANP)

promotes excretion of Na+ followed by water

excretion-increases urine output

Angiotensin II- decreases GFR- decreases urine

output

Regulation of Water Output


Edema occurs when excess interstitial fluid

collects, causing swelling in the tissues. Edema

occurs anytime filtration exceeds reabsorption

The most important causes of edema are:

increased blood pressure (increased blood

hydrostatic pressure)

an increase in the capillary permeability

a decrease in COP (decreased plasma proteins)

an obstruction in lymphatic drainage

Edema


Water is the universal solvent Solutes classified into: Nonelectrolytes –do not dissociate in solution e.g.

glucose, lipids, urea Electrolytes –dissociate into ions in solution e.g.

salts, acids, bases Electrolytes have greater osmotic power and

cause fluid shifts ( because more number of particles in solution)

Electrolytes expressed in milliequivalents per liter (mEq/L)

◦ Sodium - 136-146 mEq/L

◦ Potassium - 3.5-5.0 mEq/L

Electrolytes


Most abundant extracellular cation accounts for most of osmolarity of ECF

Sodium salts account for 90-95% of all

solutes in ECF

Regulation of Na-water balance is linked to

BP & blood volume regulation

Sodium


Sodium reabsorption in the kidney 65% of sodium in filtrate is reabsorbed in the

proximal tubules 25% is reabsorbed in the loops of Henle

When aldosterone levels are high, all of remaining Na+ can be reabsorbed in DCT & CDs-water follows if tubule permeability has been increased with ADH

When aldosterone is inhibited- no more Na reabsorbed in DCT & CDs

ANP: decreases Na reabsorption- causing sodium loss followed by water loss in urine

Regulation of Sodium Balance: Aldosterone


Cl- is most prevalent extracellular anion

Regulation:

In the kidney negatively charged chloride

passively follows the positively charged Na+

Helps balance anions in different

compartments e.g. chloride shift across red

blood cells with HCO3 ions

It plays a role in forming HCl in the stomach

Chloride


K+ is the most abundant cation in intracellular fluid

Exchanged for H+ across cells to help regulate pH of

body fluids

Helps establish resting membrane potential &

repolarize nerve & muscle cells

Regulation: mainly by aldosterone which

stimulates principal cells to increase K+ secretion

into the urine

Abnormal plasma K+ levels adversely affect cardiac

and neuromuscular function

Potassium


Hyperkalemia- high K+ concentration

Can be caused by crush injury, hemolytic

anemia's, (K+ released from ruptured cells)

Can cause death by abnormal cardiac rhythms

Hypokalemia- low K+ concentration

Can be caused by excessive vomiting, diarrhea

Nerve & muscle cells become less excitable, can

cause muscle paralysis

Clinical Application


Forms the blood acid-base buffer system with carbonic

acid.

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 of collecting ducts generally reabsorb

HCO3-, but can excrete excess in the urine if levels high

Bicarbonate (HCO3-)


98% located in bones and teeth.

Important role in blood clotting, neurotransmitter

release, muscle contraction

Regulated by parathyroid hormone:

1.Stimulates osteoclasts to release calcium

from bone

2. Increases production of calcitriol (VitD)-

which promotes Ca++ absorption from GI tract

3.Increases reabsorption of Ca in kidneys

Calcium


Present as calcium phosphate salts in bones and

teeth, and in phospholipids, ATP, DNA and RNA

Is most important intracellular anion and acts as

buffer of H+ inside cells and in urine

Regulation: plasma levels are regulated by

parathyroid hormone resorption of bone releases phosphate in the kidney, PTH increase phosphate

excretion, lowering blood phosphate Calcitriol increases GI absorption of phosphate

Phosphate


Individuals at risk for fluid and electrolyte

imbalances include:

those dependent on others for fluid and food needs

those undergoing medical treatment involving

intravenous infusions, drainage, suction, and urinary

catheters

those receiving diuretics

individuals with burns, and those with altered states

of consciousness

Clinical Application


Normal pH of blood

Arterial blood is 7.4

Venous blood is 7.35

Alkalosis– arterial blood pH rises above 7.45

Acidosis– arterial pH drops below 7.35

Acid-Base Balance


Produced from metabolic wastes:

e.g., lactic acid from anaerobic cellular respiration

e.g., phosphoric acid from nucleic acid metabolism

e.g. ketoacids from fat metabolism

Regulated by kidney through reabsorption and elimination

of HCO3- and H+

Volatile acid:

Carbonic acid produced when carbon dioxide combines with

water

◦ CO2 + H2O H2CO H+ + HCO3-

Regulated by respiratory system through respiratory rate

Sources of Acids


Concentration of hydrogen ions in blood is

regulated by:

Chemical buffer systems – act within

seconds

The respiratory system– acts within 1-3

minutes

Renal mechanisms– require hours to days

to effect pH changes

pH Regulation


Chemical Buffer Systems- General

Concepts Strong acids – dissociate

completely-release all their H+ in

water

Weak acids – dissociate partially

in water- act as buffers

Strong bases – dissociate easily in

water and quickly tie up H+

Weak bases – accept H+ more

slowly (e.g., HCO3¯)- act as buffers


Chemical Buffer Systems A chemical buffer consists of a weak acid and a

weak base

Resist pH changes when a strong acid or base is

added by

converting strong acids or bases into weak acids &

weak bases

Three major chemical buffer systems

Bicarbonate buffer system

Phosphate buffer system

Protein buffer system


Bicarbonate buffer system is a mixture of

carbonic acid (H2CO3) a weak acid , and

bicarbonate (HCO3 )

a weak base This system is the most important ECF

buffer (blood, tissue fluids) The HCO3 ion levels in ECF are regulated by

the kidney, the H2CO3 levels by the lungs

Carbonic acid-Bicarbonate Buffer System


Bicarbonate Buffer System- contd.

If there is an excess of H+ due to a strong acid the

buffer system acts by:

H+ released by strong acid combine with the HCO3

ions to form carbonic acid; a weak acid which then

replaces the strong acid H+ + HCO3¯

H2CO3

Therefore the pH of the solution decreases only

slightly If there is a shortage of H+ due to a strong base

which ties up H+: the carbonic acid dissociates into H+ and bicarbonate

ions The weak bicarbonate base replaces the strong base


Phosphate buffer system

Important intracellular buffer, but also acts to

buffer acids in the urine

Works the same way as the carbonic acid-

bicarbonate system

Protein buffer system

Buffer in cells & in plasma

Hemoglobin is an important buffer which binds H+

released from H2CO3 formed during transport of CO2

Albumin is main protein buffer in plasma

Chemical Buffer Systems


Respiratory Regulation of pH: Exhalation of Carbon Dioxide

Respiratory system acts by changing the rate and

depth of breathing, CO2 is exhaled or retained,

and blood pH is corrected

CO2 formed by cell respiration enters RBCs & is

converted to HCO3¯ for transport in plasma

CO2 + H2O H2CO3 H+ + HCO3¯

Normally released H+ are buffered by Hb

An increase in CO2 , increases H+ concentration, thus lowers the pH

(makes body fluids more acidic)

An decrease in CO2 , decreases H+ concentration, thus raises the pH

(makes body fluids more alkaline)


Changes in rate & depth of breathing can alter the pH

within minutes:

An increase in the rate and depth of breathing

causes more carbon dioxide to be exhaled,

lowering pCO2 levels in blood; thereby increasing

pH.

A decrease in respiration rate and depth means

that less carbon dioxide is exhaled, increasing

CO2 levels in blood causing the blood pH to fall.

Respiratory Regulation of pH: Exhalation of Carbon Dioxide


pH & rate & depth of

breathing interact by a

negative feedback loop:

Low pH detected by

chemoreceptors in

medulla, carotid & aortic

bodies

Increases rate & depth of

breathing; more CO2

exhaled: blood pH goes

back up to normal


Need for Renal Mechanisms

Chemical buffers prevent changes in pH, but they cannot eliminate acids & bases from the body

The body produces nonvolatile acids such as lactic acids, uric acid, ketone bodies etc, unlike volatile acid H2CO3, they cannot be removed by lungs- have to be removed by the kidneys

Therefore although slow acting the ultimate acid-base regulatory organs are the kidneys


Kidneys control acid base balance by excreting: Acidic urine– reducing the amount of acid in

ECF Alkaline urine- removing base in urine

The kidneys regulates acid base balance mainly

by reabsorption of HCO3¯ & secretion of H+:

The kidneys prevent the loss of filtered HCO3¯

conserving this important buffer

They secrete H+ to get rid of excess acid

Both the PCT & collecting ducts secrete H+ and

reabsorb HCO3¯

Acid-Base Balance


Within PCT cells H+ and

bicarbonate ion produced

Na+/H+ antiporters used to

secrete H+ while bicarbonate

reabsorbed into peritubular capillaries

H+ secreted into the tubular

fluid, combines with filtered

bicarbonate to form CO2 &

water

H+ secreted but not actually

excreted in urine

Kidney excretion of H+ -PCT


Within intercalated cells H+ and

bicarbonate ion are produced

The intercalated cells have proton

pumps (H+ ATPases) that secrete H+

into the tubular fluid, while HCO3–

reabsorbed

H+ secreted is actually excreted in

urine; can create very acidic urine

If pH of blood too alkaline other

intercalated cells can secrete HCO3–

and reabsorb H+

Kidney excretion of H+ in Collecting ducts


Respiratory Acidosis and Alkalosis Respiratory system itself the cause of pH

imbalance; caused by changed levels of pCO2

Respiratory acidosis: Arterial blood pCO2 above 45mmHg Occurs when a person breathes shallowly, or gas

exchange is hampered by diseases such as pneumonia, emphysema, pulmonary edema

CO2 accumulates in blood-rise in pCO2 causes fall in pH

Respiratory alkalosis: Arterial blood pCO2 below 35mmHg CO2 is eliminated faster than it is produced- pH

becomes alkaline Common result of hyperventilation- stress, panic,

stroke

Renal compensation can help keep pH within normal range by controlling H+ secretion& HCO3 reabsorption


Metabolic Acidosis and Alkalosis Metabolic pH imbalances – from

disturbances in plasma HCO3¯ Include pH imbalances except those caused by

abnormal blood carbon dioxide levels Metabolic Acidosis Low bicarbonate levels , low pH Causes- excessive loss of bicarbonate ions in diarrhea accumulation of lactic acid, keto acids in diabetic

crisis kidney failure- failing kidney unable to excrete H+ Respiratory compensation through

hyperventilation may bring pH into normal range


Metabolic Alkalosis

Rising blood pH and bicarbonate levels indicate

metabolic alkalosis

Typical causes are:

Vomiting of the acid contents of the stomach

Intake of excess base (e.g., from antacids)

Gastric suctioning

Respiratory compensation through hypoventilation

may bring pH into normal range

Metabolic Acidosis and Alkalosis

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Chapter 27