Chapter 27 - Fluid, Electrolyte, and Acid-Base Balance

 

Body Fluids

•      Intracellular

•    All fluids inside cells of body

•    About 40% of total body weight

•      Extracellular

•    All fluids outside cells

•    About 20% of total body weight

•    Subcompartments

•   Interstitial fluid and plasma; lymph, CSF, synovial fluid

 

Fluid Compartments

•      Water occupies two main fluid compartments

•      Intracellular fluid (ICF) – about two thirds by volume, contained in cells

•      Extracellular fluid (ECF) – consists of two major subdivisions

•    Plasma – the fluid portion of the blood

•    Interstitial fluid (IF) – fluid in spaces between cells

•      Other ECF – lymph, cerebrospinal fluid, eye humors, synovial fluid, serous fluid, and gastrointestinal secretions

 

Composition of Body Fluids

•      Water is the universal solvent

•      Solutes are broadly classified into:

•    Electrolytes – inorganic salts, all acids and bases, and some proteins

•    Nonelectrolytes – examples include glucose, lipids, creatinine, and urea

•      Electrolytes have greater osmotic power than nonelectrolytes

•      Water moves according to osmotic gradients

 

Body Water Content

•      Infants have low body fat, low bone mass, and are 73% or more water

•      Total water content declines throughout life

•      Healthy males are about 60% water; healthy females are around 50%

•      This difference reflects females’:

•    Higher body fat

•    Smaller amount of skeletal muscle

•      In old age, only about 45% of body weight is water

 

Extracellular and Intracellular Fluids

•      Each fluid compartment of the body has a distinctive pattern of electrolytes

•      Extracellular fluids are similar (except for the high protein content of plasma)

•    Sodium is the chief cation

•    Chloride is the major anion

•      Intracellular fluids have low sodium and chloride

•    Potassium is the chief cation

•    Phosphate is the chief anion

•      Sodium and potassium concentrations in extra- and intracellular fluids are nearly opposites

•      This reflects the activity of cellular ATP-dependent sodium-potassium pumps

•      Electrolytes determine the chemical and physical reactions of fluids

•      Proteins, phospholipids, cholesterol, and neutral fats account for:

•    90% of the mass of solutes in plasma

•    60% of the mass of solutes in interstitial fluid

•    97% of the mass of solutes in the intracellular compartment

 

Fluid Movement Among Compartments

•      Compartmental exchange is regulated by osmotic and hydrostatic pressures

•      Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream

•      Exchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranes

•      Two-way water flow is substantial

 

Water Balance

•      To remain properly hydrated, water intake must equal water output

•      Water intake sources

•    Ingested fluid (60%) and solid food (30%)

•    Metabolic water or water of oxidation (10%)

•      Water output:

•    Urine (61%) and feces (4%)

•    Evaporation (28%), sweat (8%)

•      Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH)

 

Water Content Regulation

•      Content regulated so total volume of water in body remains constant

•      Kidneys primary regulator of water excretion

•      Regulation processes

•     Osmosis

•     Osmolality

•     Baroreceptors

•     Learned behavior

•      Sources of water

•     Ingestion

•     Cellular metabolism

•      Routes of water loss

•     Urine

•     Evaporation

•   Perspiration

•   Respiratory passages

•     Feces

 

Regulation of Water Intake

•      The hypothalamic thirst center is stimulated by:

•    Decreases in plasma volume of 10%

•    Increases in plasma osmolality of 1–2%

•      Thirst is quenched as soon as we begin to drink water

•      Feedback signals that inhibit the thirst centers include:

•    Damping of mucosa of the mouth

•    Moistening of the throat

•    Activation of stomach and intestinal stretch receptors

 

Regulation of Water Output

•      Obligatory water losses include:

•    Insensible water losses from lungs and skin

•    Water that accompanies undigested food residues in feces

•      Obligatory water loss reflects the facts that:

•    Kidneys excrete 900–1200 mOsm of solutes to maintain blood homeostasis

•    Urine solutes must be flushed out of the body in water

 

Disorders of Water Balance: Dehydration

•      Water loss exceeds water intake and the body is in negative fluid balance

•      Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse

•      Signs and symptoms: cottonmouth, thirst, dry flushed skin, and oliguria

•      Prolonged dehydration may lead to weight loss, fever, and mental confusion

•      Other consequences include hypovolemic shock and loss of electrolytes

 

Disorders of Water Balance: Hypotonic Hydration

•      Renal insufficiency or an extraordinary amount of water ingested quickly can lead to cellular overhydration, or water intoxication

•      ECF is diluted – sodium content is normal but excess water is present

•      The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling

•      These events must be quickly reversed to prevent severe metabolic disturbances, particularly in neurons

 

Extracellular Fluid Osmolality

•      Osmolality

•     Adding or removing water from a solution changes this

 

•      Increased osmolality

•     Triggers thirst and ADH secretion

•      Decreased osmolality

•     Inhibits thirst and ADH secretion

 

Regulation of ECF Volume

•      Mechanisms

•     Neural

•     Renin-angiotensin-aldosterone

•     Antidiuretic hormone (ADH)

•     Atrial natriuretic hormone (ANH)

•      Increased ECF results in

•      Decreased aldosterone secretion

•      Increased ANH secretion

•      Decreased ADH secretion

•      Decreased sympathetic stimulation

•      Decreased ECF results in

•      Increased aldosterone secretion

•      Decreased ANH secretion

•      Increased ADH secretion

•      Increased sympathetic stimulation

 

Regulation of Electrolytes in ECF

•      Electrolytes

•     Molecules or ions with an electrical charge

•   Water ingestion adds electrolytes to body

•   Kidneys, liver, skin, lungs remove from body

•     Concentration changes only when growing, gaining or losing weight

•      Na+ Ions

•     Dominant ECF cations

•     Responsible for 90-95% of osmotic pressure

•      Regulation of Na+ ions

•     Kidneys major route of excretion

•     Small quantities lost in sweat

•      Terms

•     Hypernatremia

•     Hyponatremia

 

Electrolyte Balance

•      Electrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balance

•      Salts are important for:

•    Neuromuscular excitability

•    Secretory activity

•    Membrane permeability

•    Controlling fluid movements

•      Salts enter the body by ingestion and are lost via perspiration, feces, and urine

 

Sodium in Fluid and Electrolyte Balance

•      Sodium holds a central position in fluid and electrolyte balance

•      Sodium salts:

•    Account for 90–95% of all solutes in the ECF

•    Contribute 280 mOsm of the total 300 mOsm ECF solute concentration

•      Sodium is the single most abundant cation in the ECF

•      Sodium is the only cation exerting significant osmotic pressure

•      The role of sodium in controlling ECF volume and water distribution in the body is a result of:

•    Sodium being the only cation to exert significant osmotic pressure

•    Sodium ions leaking into cells and being pumped out against their electrochemical gradient

•      Sodium concentration in the ECF normally remains stable

•      Changes in plasma sodium levels affect:

•    Plasma volume, blood pressure

•    ICF and interstitial fluid volumes

•      Renal acid-base control mechanisms are coupled to sodium ion transport

 

Influence and Regulation of ADH

•      Water reabsorption in collecting ducts is proportional to ADH release

•      Low ADH levels produce dilute urine and reduced volume of body fluids

•      High ADH levels produce concentrated urine

•      Hypothalamic osmoreceptors trigger or inhibit ADH release

•      Factors that specifically trigger ADH release include prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns

 

Regulation of Sodium Balance: Aldosterone

•      Sodium reabsorption

•    65% of sodium in filtrate is reabsorbed in the proximal tubules

•    25% is reclaimed in the loops of Henle

•      When aldosterone levels are high, all remaining Na+ is actively reabsorbed

•      Water follows sodium if tubule permeability has been increased with ADH

•      The renin-angiotensin mechanism triggers the release of aldosterone

•      This is mediated by the juxtaglomerular apparatus, which releases renin in response to:

•    Sympathetic nervous system stimulation

•    Decreased filtrate osmolality

•    Decreased stretch (due to decreased blood pressure)

•      Renin catalyzes the production of angiotensin II, which prompts aldosterone release

•      Adrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECF

•      Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly

 

Atrial Natriuretic Peptide (ANP)

•      Reduces blood pressure and blood volume by inhibiting:

•    Events that promote vasoconstriction

•    Na+ and water retention

•      Is released in the heart atria as a response to stretch (elevated blood pressure)

•      Has potent diuretic and natriuretic effects

•      Promotes excretion of sodium and water

•      Inhibits angiotensin II production

 

Regulation of Other Ions

•      Chloride ions

•     Predominant anions in ECF

•      Magnesium ions

•     Capacity of kidney to reabsorb is limited

•     Excess lost in urine

•     Decreased extracellular magnesium results in greater degree of reabsorption

•      Potassium ions

•     Maintained in narrow range

•     Affect resting membrane potentials

•     Aldosterone increases amount secreted

 

Regulation of Anions (Chloride)

•      Chloride is the major anion accompanying sodium in the ECF

•      99% of chloride is reabsorbed under normal pH conditions

•      When acidosis occurs, fewer chloride ions are reabsorbed

•      Other anions have transport maximums and excesses are excreted in urine

 

Regulation of Potassium Balance

•      Relative ICF-ECF potassium ion concentration affects a cell’s resting membrane potential

•    Excessive ECF potassium decreases membrane potential

•    Too little K+ causes hyperpolarization and nonresponsiveness

•      Hyperkalemia and hypokalemia can:

•    Disrupt electrical conduction in the heart

•    Lead to sudden death

•      Hydrogen ions shift in and out of cells

•    Leads to corresponding shifts in potassium in the opposite direction

•    Interferes with activity of excitable cells

 

Regulatory Site: Cortical Collecting Ducts

•      Less than 15% of filtered K+ is lost to urine regardless of need

•      K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate

•      Excessive K+ is excreted over basal levels by cortical collecting ducts

•      When K+ levels are low, the amount of secretion and excretion is kept to a minimum

•      Type A intercalated cells can reabsorb some K+ left in the filtrate

 

Influence of Aldosterone

•      Aldosterone stimulates potassium ion

•      In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted

•      Increased K+ in the ECF around the adrenal cortex causes:

•    Release of aldosterone

•    Potassium secretion

•      Potassium controls its own ECF concentration via feedback regulation of aldosterone release

 

Regulation of Calcium Ions

•      Regulated within narrow range

•     Elevated extracellular levels prevent membrane depolarization

•     Decreased levels lead to spontaneous action potential generation

•      Terms

•     Hypocalcemia

•     Hypercalcemia

•      PTH increases Ca2+ extracellular levels and decreases extracellular phosphate levels

•      Vitamin D stimulates Ca2+ uptake in intestines

•      Calcitonin decreases extracellular Ca2+ levels

 

Regulation of Calcium

•      Ionic calcium in ECF is important for:

•    Blood clotting

•    Cell membrane permeability

•    Secretory behavior

•      Hypocalcemia:

•    Increases excitability

•    Causes muscle tetany

•      Hypercalcemia:

•    Inhibits neurons and muscle cells

•    May cause heart arrhythmias

•      Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin

 

Influence of Calcitonin

•      Released in response to rising blood calcium levels

•      Calcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible

 

Regulation of Calcium and Phosphate

•      PTH promotes increase in calcium levels by targeting:

•    Bones – PTH activates osteoclasts to break down bone matrix

•    Small intestine – PTH enhances intestinal absorption of calcium

•    Kidneys – PTH enhances calcium reabsorption and decreases phosphate reabsorption

•      Calcium reabsorption and phosphate excretion go hand in hand

•      Filtered phosphate is actively reabsorbed in the proximal tubules

•      In the absence of PTH, phosphate reabsorption is regulated by its transport maximum and excesses are excreted in urine

•      High or normal ECF calcium levels inhibit PTH secretion

•    Release of calcium from bone is inhibited

•    Larger amounts of calcium are lost in feces and urine

•    More phosphate is retained

 

Regulation of Phosphate Ions

•      Under normal conditions, reabsorption of phosphate occurs at maximum rate in the nephron

•      An increase in plasma phosphate increases amount of phosphate in nephron beyond that which can be reabsorbed; excess is lost in urine

 

Regulation of Magnesium Balance

•      Magnesium is the second most abundant intracellular cation

•      Activates coenzymes needed for carbohydrate and protein metabolism

•      Plays an essential role in neurotransmission, cardiac function, and neuromuscular activity

•      There is a renal transport maximum for magnesium

•      Control mechanisms are poorly understood

 

Homeostatic Imbalances

•      Hypocalcemia – reduced ionic calcium depresses the heart

•      Hypercalcemia – dramatically increases heart irritability and leads to spastic contractions

•      Hypernatremia – blocks heart contraction by inhibiting ionic calcium transport

•      Hyperkalemia – leads to heart block and cardiac arrest

 

Acids and Bases and Buffers

•      Acids

•     Release H+  into  solution

•      Bases

•     Remove H+ from solution

•      Acids and bases

•     Grouped as strong or weak

•      Buffers: Resist changes in pH

•     When H+ added, buffer removes

•     When H+ removed, buffer replaces

•      Types of buffer systems

•     Carbonic acid/bicarbonate

•     Protein

•     Phosphate

 

Acid-Base Balance

•      Normal pH of body fluids

•    Arterial blood is 7.4

•    Venous blood and interstitial fluid is 7.35

•    Intracellular fluid is 7.0

•      Alkalosis or alkalemia – arterial blood pH rises above 7.45

•      Acidosis or acidemia – arterial pH drops below 7.35 (physiological acidosis)

 

Acidosis and Alkalosis

•      Acidosis: pH body fluids below 7.35

•    Respiratory: Caused by inadequate ventilation

•    Metabolic: Results from all conditions other than respiratory that decrease pH

•      Alkalosis: pH body fluids above 7.45

•    Respiratory: Caused by hyperventilation

•    Metabolic: Results from all conditions other than respiratory that increase pH

•      Compensatory mechanisms

 

Chemical Buffer Systems

•      Strong acids – all their H+ is dissociated completely in water

•      Weak acids – dissociate partially in water and are efficient at preventing pH changes

•      Strong bases – dissociate easily in water and quickly tie up H+

•      Weak bases – accept H+ more slowly (e.g., HCO3― and NH3)

•      One or two molecules that act to resist pH changes when strong acid or base is added

•      Three major chemical buffer systems

•    Bicarbonate buffer system

•    Protein buffer system

•    Phosphate buffer system

•      Any drifts in pH are resisted by the entire chemical buffering system

 

Bicarbonate Buffer System

•      A mixture of carbonic acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates work as well)

•      If strong acid is added:

•    Hydrogen ions released combine with the bicarbonate ions and form carbonic acid (a weak acid)

•    The pH of the solution decreases only slightly

•      If strong base is added:

•    It reacts with the carbonic acid to form sodium bicarbonate (a weak base)

•    The pH of the solution rises only slightly

•      This system is the only important ECF buffer

 

Protein Buffer System

•      Plasma and intracellular proteins are the body’s most plentiful and powerful buffers

•      Some amino acids of proteins have:

•    Free organic acid groups (weak acids)

•    Groups that act as weak bases (e.g., amino groups)

•      Amphoteric molecules are protein molecules that can function as both a weak acid and a weak base

 

Phosphate Buffer System

•      Nearly identical to the bicarbonate system

•      Its components are:

•    Sodium salts of dihydrogen phosphate (H2PO4―), a weak acid

•    Monohydrogen phosphate (HPO42―), a weak base

•      This system is an effective buffer in urine and intracellular fluid

 

Respiratory and Renal Compensations

•      Acid-base imbalance due to the inadequacy of a physiological buffer system is compensated for by the other system

•    The respiratory system will attempt to correct metabolic acid-base imbalances

•    The kidneys will work to correct imbalances caused by respiratory disease

 

Physiological Buffer Systems

•      The respiratory system regulation of acid-base balance is a physiological buffering system

•      There is a reversible equilibrium between:

•    Dissolved carbon dioxide and water

•    Carbonic acid and the hydrogen and bicarbonate ions

 

CO2 + H2O « H2CO3 « H+ + HCO3

 

Respiratory Regulation of Acid-Base Balance

•      Respiratory regulation of pH is achieved through carbonic acid/bicarbonate buffer system

•     As carbon dioxide levels increase, pH decreases

•     As carbon dioxide levels decrease, pH increases

•     Carbon dioxide levels and pH affect respiratory centers

•   Hypoventilation increases blood carbon dioxide levels

•   Hyperventilation decreases blood carbon dioxide levels

 

Respiratory Compensation

•      In metabolic acidosis:

•    The rate and depth of breathing are elevated

•    Blood pH is below 7.35 and bicarbonate level is low

•    As carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal

•      In respiratory acidosis, the respiratory rate is often depressed and is the immediate cause of the acidosis

•      In metabolic alkalosis:

•    Compensation exhibits slow, shallow breathing, allowing carbon dioxide to accumulate in the blood

•      Correction is revealed by:

•    High pH (over 7.45) and elevated bicarbonate ion levels

•      Rising PCO2

 

Renal Regulation of Acid-Base Balance

•      Secretion of H+ into filtrate and reabsorption of HCO3- into ECF cause extracellular pH to increase

•      HCO3- in filtrate reabsorbed

•      Rate of H+ secretion increases as body fluid pH decreases or as aldosterone levels increase

•      Secretion of H+ inhibited when urine pH falls below 4.5

 

Renal Mechanisms of Acid-Base Balance

•      The most important renal mechanisms for regulating acid-base balance are:

•    Conserving (reabsorbing) or generating new bicarbonate ions

•    Excreting bicarbonate ions

•      Losing a bicarbonate ion is the same as gaining a hydrogen ion; reabsorbing a bicarbonate ion is the same as losing a hydrogen ion

 

Reabsorption of Bicarbonate

•      Carbon dioxide combines with water in tubule cells, forming carbonic acid

•      Carbonic acid splits into hydrogen ions and bicarbonate ions

•      For each hydrogen ion secreted, a sodium ion and a bicarbonate ion are reabsorbed by the PCT cells

•      Secreted hydrogen ions form carbonic acid; thus, bicarbonate disappears from filtrate at the same rate that it enters the peritubular capillary blood

•      Carbonic acid formed in filtrate dissociates to release carbon dioxide and water

•      Carbon dioxide then diffuses into tubule cells, where it acts to trigger further hydrogen ion secretion

 

Generating New Bicarbonate Ions

•      Two mechanisms carried out by type A intercalated cells generate new bicarbonate ions

•      Both involve renal excretion of acid via secretion and excretion of hydrogen ions or ammonium ions (NH4+)

 

Generating New Bicarbonate Ions Using Hydrogen Ion Excretion

•      Dietary hydrogen ions must be counteracted by generating new bicarbonate

•      The excreted hydrogen ions must bind to buffers in the urine (phosphate buffer system)

•      Intercalated cells actively secrete hydrogen ions into urine, which is buffered and excreted

•      Bicarbonate generated is:

•    Moved into the interstitial space via a cotransport system

•    Passively moved into the peritubular capillary blood

 

Generating New Bicarbonate Ions Using Hydrogen Ion Excretion

•      In response to acidosis:

•    Kidneys generate bicarbonate ions and add them to the blood

•    An equal amount of hydrogen ions are added to the urine

 

Generating New Bicarbonate Ions Using Ammonium Ion Excretion

•      This method uses ammonium ions produced by the metabolism of glutamine in PCT cells

•      Each glutamine metabolized produces two ammonium ions and two bicarbonate ions

•      Bicarbonate moves to the blood and ammonium ions are excreted in urine

 

Bicarbonate Ion Secretion

•      When the body is in alkalosis, type B intercalated cells:

•    Exhibit bicarbonate ion secretion

•    Reclaim hydrogen ions and acidify the blood

•      The mechanism is the opposite of type A intercalated cells and the bicarbonate ion reabsorption process

•      Even during alkalosis, the nephrons and collecting ducts excrete fewer bicarbonate ions than they conserve

 

Renal Compensation

•      To correct respiratory acid-base imbalance, renal mechanisms are stepped up

•      In acidosis

•    High PCO2 and high bicarbonate levels

•   The high PCO2 is the cause of acidosis

•   The high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis

•      In alkalosis

•    Low PCO2 and high pH

•   The kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it

 

Assessing Acid-Base Balance Using Blood Values

•      Note the pH: this indicates if the person is in acidosis (pH<7.35) or alkalosis (pH>7.45), but it does not tell the cause

•      Check the PCO2: excessively high or low PCO2 indicate

•    Whether the condition is caused by the respiratory system

•    Whether the respiratory system is compensating

•      Check the bicarbonate level: if the respiratory system is not the cause, it is a metabolic condition

 

Respiratory Acidosis and Alkalosis

•      Result from failure of the respiratory system to balance pH

•      PCO2 is the single most important indicator of respiratory inadequacy

•      Normal PCO2

•    Fluctuates between 35 and 45 mm Hg

•    Values above 45 mm Hg signal respiratory acidosis

•    Values below 35 mm Hg indicate respiratory alkalosis

•      Respiratory acidosis is the most common cause of acid-base imbalance

•    Occurs when a person breathes shallowly, or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis, or emphysema

•      Respiratory alkalosis is a common result of hyperventilation

 

Metabolic Acidosis

•      All pH imbalances except those caused by abnormal blood carbon dioxide levels

•      Metabolic acid-base imbalance – bicarbonate ion levels above or below normal (22–26 mEq/L)

•      Metabolic acidosis is the second most common cause of acid-base imbalance

•    Typical causes are ingestion of too much alcohol and excessive loss of bicarbonate ions

•    Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure

•      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)

•    Constipation, in which excessive bicarbonate is reabsorbed

 


Lecture Outline - Fluid, Electrolyte, and Acid-Base Balance

 

       I.   Body Fluids

A. Body Water Content

B. Fluid Compartments

1. Intracellular Fluid

2. Extracellular Fluid

a. Plasma

b. Interstitial Fluid

C.      Composition of Fluids

1. Solutes

a. Electrolytes

b. Nonelectrolytes

2. Comparison of Extracellular and Intracellular Fluids

D. Fluid Movement Among Compartments

      II.   Water Balance

A. Regulation of Water Intake: The Thirst Mechanism

1. The Thirst Mechanism

B. Regulation of Water Output

1. Obligatory Water Losses

C.      Disorders of Water Balance

1. Dehydration

2. Hypotonic Hydration

3. Edema

    III.   Electrolyte Balance

A. Central Role of Sodium in Fluid and Electrolyte Balance

B. Regulation of Sodium Balance

1. Influence and Regulation of Aldosterone

2. Cardiovascular System Baroreceptors

3. Influence and Regulation of ADH

4. Influence and Regulation of Atrial Natriuretic Factor

5. Influence of Other Hormones

a. Female Sex Hormones

b. Glucocorticoids

C.      Regulation of Potassium Balance

1. Regulatory Site: The Cortical Collecting Duct

2. Influence of Plasma Potassium Concentration

3. Aldosterone Levels

D. Regulation of Calcium and Phosphate Balance

1.  Influence of Parathyroid Hormone

a. Bones

b. Small Intestine

c. Kidneys

2. Influence of Calcitonin

E. Regulation of Magnesium Balance

F. Regulation of Anions

    IV.   Acid-Base Balance

A. Introduction

1. Alkalosis

2. Acidosis

B. Chemical Buffer Systems

1. Bicarbonate Buffer System

2. Phosphate Buffer System

3. Protein Buffer System

V. Physiological Buffer Systems

A. Respiratory System Regulation of Hydrogen Ion Concentration

B. Renal Mechanisms of Acid-Base Balance

1. Regulation of Hydrogen Ion Secretion

2. Conserving Filtered Bicarbonate Ions: Bicarbonate Reabsorption

3. Generating New Bicarbonate Ions

a. Via Excretion of Buffered H+

b. Via NH4+ Excretion

4. Bicarbonate Ion Secretion

C.      Abnormalities of Acid-Base Balance

1. Respiratory Acidosis or Alkalosis

a. Respiratory Acidosis

b. Respiratory Alkalosis

2. Metabolic Acidosis or Alkalosis

a. Metabolic Acidosis

b. Metabolic Alkalosis

3.      Effects of Acidosis or Alkalosis

4.      Respiratory and Renal Compensation