acid-base balance
internal amount of a substance = Pool
Input : external environment/ produced in body (metabolism)
output : excreted/ used up in body
-to remain stable must balance (central to homeostasis, in this case blood H+ homeostasis)
three states of total-body balance are possible
- negative balance (loss>gain)
- positive balance (gain >loss)
- stable balance (gain=loss)
sources of hydrogen gain
- hypoventilation
- produced in metabolism
- loss of bicarbonate in diarrhea, urine
sources of hydrogen loss
- hyperventilation
- used in metabolism
- loss in vomit, urine
acid-base balance
-Normal pH arterial blood 7.35 to 7.45
Alkalosis > 7.45 →increased pH/ decreased H+
Acidosis <7.35 → decreased pH/increased H+
pH limit for sustaining life :
-<6.8 : nervous system depression; can lead to coma/death
→7.8 nervous system overexcited; can lead to convulsion/respiratory arrest
Buffering - 1st line defense
(immediate response)
chemical buffer : can reversibly bind hydrogen
reaction : buffer + H+ ←→ HBuffer
- -does not eliminate hydrogen from body or add it to body*
- try to stabilize hydrogen concentration against changes in either direction
Bicarbonate buffer
(major extracellular buffer)
H2CO3 ←→H+ + HCO3-
carbonic acid ←→hydrogen ion + Bicarbonate ion
- plasma H+ concentration decreases (alkalosis) → carbonic acid releases hydrogen and bicarbonate (reaction to right)
- plasma H+ concentration increases (acidosis) - hydrogen combines with bicarbonate to form carbonic acid (reaction to left)
Alkaline reserve = amount of bicarbonate in body
Phosphate buffer
(one of major intracellular buffers)
H2PO-4 ←→ H+ + HPO2-4
Dihydrogen phosphate ←→ Hydrogen Ion + Monohydrogen phosphate
-Plasma H+ concentration decreases (alkalosis) - dihydrogen phosphate releases hydrogen (reaction to right)
-Plasma H+ concentration increases (acidosis) - monohydrogen phosphate binds hydrogen (reaction to the left)
Protein buffer (one of major intracellular buffers)
Hb-H←→ H+ + Hb
Deoxyhemoglobin ←→ Hydrogen Ion + Hemoglobin
- plasma H+ concentration decreases (alkalosis) -carboxyl end of protein releases hydrogen (reaction to right)
- plasma H+ concentration increases (acidosis) - amino end of protein binds hydrogen (reaction to left)
Respiratory mechanism - 2nd line of defense (minutes)
-lungs react via ventilation (“breathing buffer”) and CO2 changes
CO2 + H2O ←→ H2CO3←→ H+ + HCO3-
Carbon dioxide + water ←→ carbonic acid ←→ hydrogen ion + bicarbonate ion
- plasma H+ concentration decreases (alkalosis), lungs response by hypoventilation to increase blood Co2 to increase H+ (reaction to right)
- Plasma H+ concentration increases (acidosis), lungs response by hyperventilation to decrease blood CO2 to decrease H+ (reaction to left)
Renal mechanism -3rd line of defense (hours/days)
- kidneys react to hydrogen and/or bicarbonate changes (urinary buffer)
- plasma H+ concentration decreases (alkalosis), kidneys’ response to excrete large quantities HCO3- to increase plasma H+ concentration
- plasma H+ concentration increases (acidosis), kidneys’ response to not excrete HCO3- in urine and produce new HCO3- to add to plasma to decrease plasma H+ concentration
renal mechanism - 3rd line of defense
bicarbonate = HCO3
- Considered filtered bicarbonate being reabsorbed even though not the actual same molecule (moving into interstitial fluid )
- Hydrogen is secreted (moved to tubular lumen)
renal mechanisms -3rd line of defense (hours/days)
-considered new bicarbonate as it does not involve filtered bicarbonate
mechanisms :
- involving filtered monohydrogen phosphate
- involving glutamate
- in either case bicarbonate is generated and reabsorbed while hydrogen is secreted
Responses to acidosis
renal mechanisms -3rd line of defense (hours/days)
responses to acidosis
- sufficient H+ secreted to reabsorb all filtered HCO3-
- More H+ secreted contributing new HCO3- as H+ is excreted bound to nonbicarbonate urinary buffers such as HPO42-
- glutamine metabolism, ammonium excretion contributing new HCO3-.
Net result : more new and reabsorbed bicarbonate than usual is added to blood, increasing plasma HCO3- and compensating for acidosis. Urine is highly acidic
Responses to alkalosis
renal mechanisms -3rd line of defense (hours/days)
- H+ secretion is inadequate to reabsorb all filtered HCO3-, so significant amounts of HCO3- are excreted in urine
- little or no excretion of H+ on nonbicarbonate urinary buffers (phosphate) so little or no new HCO3-
- glutamine metabolism, ammonium excretion decreased so little or no new HCO3-
Net result : plasma HCO3- is decreased, compensating for alkalosis. Urine is Alkaline
acid-base imbalances
assessment
If change has a respiratory cause -CO2 change
- respiratory acidosis (high CO2) vs. respiratory alkalosis (Low CO2)
If change has a metabolic cause - bicarbonate change (HCO3)
-metabolic acidos (low bicarbonate) vs. metabolic alkalosis (high bicarbonate)
sources
respiratory (normal : inverted acidosis =increased Co2)
-acidosis : hypoventilation, emphysema, pneumonia
-alkalosis : hyperventilation, stress, pain
Metabolic (not normal : not inverted)
-acidosis : exercise, diabetes, diarrhea, ketosis, excess alcohol
-alkalosis : vomiting, alkaline drug ingestion
respiratory acidosis
carbon dioxide builds up in blood; increased production of hydrogen (blood too acidic)
respiratory alkalosis
carbon dioxide in blood lower than normal ; decreased production of hydrogen (blood too alkaline)
metabolic acidosis
excessive hydrogen in blood not from Co2 (blood too acidic)
metabolic alkalosis
reduction of hydrogen in blood due to deficiency of non-carbonic acids (blood too alkaline)
