Ch 26 Fluid, Electrolyte, and Acid-Base Balance

Body Fluid Compartments

• Intracellular fluid (ICF)

• Extracellular fluid (ECF)

Intracellular fluid (ICF)

• ~66% of total body water found here

• K+, proteins, hydrogen phosphate

Extracellular fluid (ECF)

• ~33% of remaining body water found here

• Two sub-compartments

• Na+, Cl-, bicarbonate

Two sub-compartments of ECF

1) Plasma

2) Interstitial fluid (IF)

Interstitial fluid (IF)

Lymph, cerebrospinal fluid, humors, serous fluid, synovial fluid

Composition of Body Fluids

• Electrolytes

• Non-electrolytes

Electrolytes

anything that dissociate into ions in water

• (+) or (-) charge

• Most abundant solutes

• More responsible for fluid shifts/movement of water

-->• Ex: inorganic salts, acids & bases, some proteins

Non-electrolytes

do not dissociate in water

• No charge

• Make up the bulk of the body fluids

• Ex: glucose, urea, lipids, etc.

Optimal body water content depends on:

• Age

• Sex

• Body fat %

Sources of water intake

• Ingested food & liquid

• Metabolic water

Sources of water output

• Insensible water loss: lungs, skin

• Sensible water loss: sweat, urine, feces

When properly hydrated,

water intake = water output

Importance of: water intake = water output

allows body to maintain osmolality of ~300 mOsm

Regulating water intake

• Hypothalamic thirst center controls the thirst mechanism, is activated by:

1) Osmoreceptors

2) Dry mouth

3) Decreasing blood volume/pressure

• Feelings of thirst stop almost as soon as we drink water

Osmoreceptors

detect changing ECF osmolality

Dry mouth

salivary glands cannot draw water from blood to produce saliva

Decreasing blood volume/pressure

~5-10% drop initiates thirst mechanism

Regulating water output

• Obligatory water loss -> the body will always lose water, even if we never drink water

-->• Insensible water loss, kidneys never stop functioning

• Urine output depends on fluid intake, diet, other sources of water loss

-->• Excess water is eliminated in urine

ADH causes aquaporins to be ___________________

inserted in collecting ducts

Release of ADH dependent on:

1) Osmoreceptors monitoring osmolality of ECF

2) Baroreceptors monitoring blood pressure

Deficiencies in ADH release

• Central diabetes insipidus

• Nephrogenic diabetes insipidus

Central diabetes insipidus

decrease in ADH produced by hypothalamus or released by posterior pituitary

Symptoms of central diabetes insipidus

polyuria (followed by polydipsia), very dilute urine, fatigue, eventual dehydration

Nephrogenic diabetes insipidus

ADH is produced and released in normal amounts, but the kidneys are unresponsive to it

Electrolyte Balance Importance

influence water movement in body, excitability of neurons , membrane permeability, etc. etc.

Salt loss

urine & feces, sweat, vomit

• Renal processes help body retain what is needed

Sodium Balance

• NaHCO3 and NaCl account for ~280 mOsm of total ECF solute

• Key player in maintaining ECF volume

Why is sodium balance a key player in maintaining ECF volume?

1) Most important in establishing osmotic gradient -> water moves with Na+

2) Plasma membranes are impermeable to Na+ -> almost always kept out of cells and in the ECF

Regulation of Na+

• Most Na+ reabsorbed in PCT and nephron loop (~85%)

• Hormonal regulation

Hormonal Regulation of Na+

1) Aldosterone

2) Atrial Natriuretic peptide (ANP)

3) Sex hormones

4) Glucocorticoids

Aldosterone

release causes increased reabsorption of Na+ in DCT & collecting ducts

• Side effect of aldosterone release: increase in ECF volume

Atrial Natriuretic peptide (ANP)

release causes decreased reabsorption of Na+

• Is diuretic and natriuretic

Sex hormones

• Estrogen exerts similar effect as aldosterone

• Progesterone is slightly diuretic

Glucocorticoids

• In high plasma levels, exerts very strong aldosterone-like effects

-->• Can contribute substantially to edema

Importance of potassium balance

1) Heavy regulation due to effect on resting membrane potential

2) Buffer

-->• K+ moves in the opposite direction of H+ to balance pH

Primary mechanism of balance

Renal

• Principal cells secrete K+ in the DCT and collecting ducts

-->• Can alter how much based on what needs to be excreted

• Type A intercalated cells can reabsorb K+ when levels are exceptionally low

-->**The kidneys are VERY limited in reabsorption capabilities K+

Potassium secretion depends on:

1) Plasma concentration

2) Aldosterone

How does potassium secretion depend on plasma concentration?

• High ECF K+ concentrations drive excess K+ into principal cells -> increased secretion & excretion of K+

• Low ECF K+ concentrations promotes reabsorption

How does potassium secretion depend on aldosterone?

• Stimulates K+ secretion

• Adrenal cortex secretes aldosterone when K+ ECF concentrations are high

• This has a limited effect -> large shifts in Na+ & volume concentrations do not affect K+ concentrations overall

--• Renal mechanisms will preserve desirable K+ concentration

Optimal pH of arterial blood is

7.35-7.45

pH 7.45 or higher

alkalosis

pH 7.35 or lower

physiological acidosis

Sources of H+ in the body

1) Ingested food

2) Metabolic processes -> lactic acid, loading of CO2, phosphoric acid, etc. etc.

Regulating H+ concentration

1) Chemical Buffer Systems

2) Respiratory Regulation of H+

3) Renal Regulation

Chemical Buffer Systems

one or more compounds that resist changesin pH when strong acids or bases are introduced

• Release H+ when pH rises, bind H+ when pH drops

• Three important buffer systems

Three important buffer systems

A) Bicarbonate buffer system

B) Phosphate buffer system

C) Protein buffer system

Bicarbonate buffer system

important for ECF

• Mixture of carbonic acid (weak acid) and bicarbonate salt (weak base)

--Bicarbonate salt + H+ = carbonic acid

--Carbonic acid + OH- = bicarbonate salt

• Conversion of strong to weak changes the pH only*slightly*

Phosphate buffer system

important for ICF and urine

• Similar to bicarbonate buffer system, but utilizes different weak acids and bases

--• Salts of dihydrogen phosphate (weak acid) and monohydrogen phosphate (weak base)

--• The end result is the same -> prevents drastic pH changes

Protein buffer system

important in ICF and blood plasma

• Carboxyl group (-COOH) can release H+ when pH rises

• Amine group (NH2) group can bind free H+ when pH decreases

• Amphoteric molecule

Amphoteric molecule

a single protein can react as either an acid or a base

• Depends on the pH of the environment

Respiratory Regulation of H+

CO2 accumulation lowers pH of blood

• Rising PCO2 activates respiratory centers

--Respiratory rate + depth increase

-- pH rises as more CO2 is blown off

• Decreasing PCO2 depress respiratory centers

--Respiratory rate + depth decrease

--pH decreases as CO2 accumulates

Renal Regulation

• Important for long-term acid base balance

• Primary mechanism of acid-base balance: adjusting amount of bicarbonate in blood

Adjusting amount of bicarbonate in blood (Renal Regulation)

A) Generating new bicarbonate

B) Secretion of bicarbonate

Generating new bicarbonate

• PCT and Type A intercalated cells of collecting ducts can generate new bicarbonate ions to be reabsorbed

--• H+ must be secreted into filtrate at the same time

Secretion of bicarbonate

• Type B intercalated cells in collecting ducts can reabsorb H+ while secreting bicarbonate ions from filtrate

• Secretion of bicarbonate is not efficient -> even in alkalosis, more bicarbonate will be reabsorbed than secreted

Homeostatic Imbalances of Acid-Base Balance

• Respiratory acidosis & alkalosis

• Metabolic acidosis & alkalosis

Respiratory acidosis

PCO2 > 45 mmHg

• Respiration is shallow/slow (hypoventilation)

• Caused by: many respiratory diseases/conditions

Respiratory alkalosis

PCO2 < 35 mm Hg

• Respiration is deep/fast (hyperventilation) • Caused by: stress/anxiety, painPCO2 < 35 mm Hg

Metabolic acidosis & alkalosis

• Any acid-base imbalance that does not involve CO2

--• Especially bicarbonate ion imbalances

Metabolic acidosis

• Low bicarbonate levels

• Common causes: excessive alcohol intake, long-term diarrhea

Metabolic alkalosis

• High bicarbonate levels

• Common causes: excessive vomiting, excessive base intake

Effects of acidosis & alkalosis

Blood pH limits are 6.8 and 7.8

-Below 6.8—CNS depression -> coma & death

-Above 7.8—overstimulated CNS

Overstimulated CNS

Muscle tetany (the bad kind), restlessness/nervousness, convulsions, death

Compensating for alkalosis & acidosis

• Kidneys or lungs can act to restore pH when other organ fails

• Respiratory compensation

• Renal compensation

Respiratory compensation

• Changes in respiratory rate & depth evident when lungs must compensate for metabolic imbalances

--• Metabolic acidosis -> respiratory rate + depth increase

--• Metabolic alkalosisrespiratory rate + depth decrease

Renal compensation

• Kidneys can compensate for acid-base imbalances of respiratory origins

• Respiratory acidosis -> kidneys conserve more bicarbonate ions

• Respiratory alkalosis -> kidneys either secrete more bicarbonate ions or simply do not reabsorb it