Lecture 7: Buffers, Acid-Base Regulation Flashcards
Normal arterial blood range pH
pH 7.38 - 7.42; slightly more acidic in venous
Normal sources of acid
- Volatile e.g. CO2 from fuel oxidation
- Fixed i.e. H+X- from metabolism of substrates e.g. sulfur/phosphorylated AAs, purines
3 lines of acid defense
- Blood buffering
- Changing ventilation (lungs, PCO2)
- Changing renal function (kidneys, HCO3-)
Henderson-Hasselbach for carbonic anhydrase Eq
pH = 6.1 + log([HCO3-] / 0.03*PCO2)
Isohydric Principle
When multiple buffers are present, all are in equilibrium with one another
Davenport diagram plot
Plots carbonic anhydrase H-H; pH vs HCO3- for given PCO2
Davenport diagram isopleths
Curve for a single PCO2; move up and down by adding/removing bicarb
How does a rise in PCO2 physiologically affect [H+] and [HCO3-]?
Buffers take away H+, so more bicarb is produced when PCO2 increases vs free H+. More buffering = more bicarb production for given ΔPCO2
Respiratory acidosis
Increased PCO2 leads to increased H+. Compensate with increased ventilation and kidney H+ excretion (more bicarb released to ECF by CA)
Respiratory alkalosis
Decreased PCO2 leading to decreased H+. Compensate w/ decreased ventilation and kidney bicarb excretion (H+ released to ECF)
Metabolic acidosis
e.g. loss of bicarb w/ diarrhea. Compensate w/ hyperventilation (kidneys restore bicarb deficit over time)
Peripheral/central chemoreceptor conflict
In metabolic acidosis peripheral chemoreceptors increase vent. due to H+ BUT central chemoreceptors then sense decreased PCO2 in CSF and decrease vent.
Overall hyperventilation can’t return blood all the way to normal pH
Metabolic alkalosis
Loss of H+ e.g. vomit, overdiuresis; peripheral chemoreceptors decrease ventilation (kidneys slowly remove bicarb excess)
