Exam #3 (Acid-Base) Flashcards
Normal range of arterial pH is
7.37 (or 7.35) to 7.42 (or 7.45)
Acidemia pH level
pH < 7.37
Alkalemia pH level
pH > 7.42
Mechanisms of maintaining normal pH
- Buffering of H+ in both ECF & ICF
- Respiratory compensation
- Renal compensation
Volatile Acid
CO2
Produced from aerobic metabolism
Non-Volatile Acid
Aka fixed acids
Sulfuric acid, phosphoric acid
Ketoacids, lactic acid, Beta-hydroxybutyric acid, glycolic acid, oxalic acid & salicylic acid
Function of buffers
Prevents change in pH when H+ ions are added to or removed from a solution
When are buffers most effective?
Most effective within 1.0 pH unit of the pK (-ve logarithm of the [H+] at which 1/2 of the acid molecules are dissociated & are undissociated) of the buffer
Extracellular buffers include
Mostly HCO3-
Phosphate: most important as a urinary buffer
Intracellular buffers include
Organic phosphates: AMP, ADP, ATP, DPG
Proteins
Hemoglobin: major buffer. Deoxyhemoglobin is better buffer than oxyhemoglobin b/c it allows for the binding of H+
Henderson-Hasselbalch Equation
Used to calculate pH
pH = -log10[H+] pK = -ve logarithm of the [H+] at which 1/2 of the acid molecules are dissociated & are undissociated [A-] = Concentration of base form of buffer; is the H acceptor [HA] = Concentration of acid form of buffer; is the H donor
In the henderson-hasselbalch equation when the concentration of A- & HA are equal,
The pH of the solution = the pH of the buffer
In a acid-base titration curve, as H+ ions are added to the solution vs as H+ ions are removed
The titration curve describes how the pH of a buffered solution changes as H ions are added/removed from it. As H+ ions are added to the solution, the HA form is produced. As H+ ions are removed, the A- form is produced.
A buffer is most effective in which portion of the acid-base titration curve?
A buffer is most effective in the linear portion of the titration curve, where the addition or removal of H+ causes little change to pH
The most effective physiologic buffer will have a pK w/
1.0 pH unit of 7.4 (7.4 ± 1.0)
Based on Henderson-Hasselbalch Equation, when the pH of the solution = pK
the concentration of HA & A are equal
As the filtered load increases what impact will it have on HCO3-
Increases in the filtered load leads to increased HCO3- reabsorption. If plasma [HCO3-] becomes high (metabolic alkalosis), then filtration will exceed reabsorption & excretion will occur
What impact does Pco2 have on filtered HCO3-
Increased Pco2 -> increased HCO3- reabsorption
Decreased Pco2 -> decreased HCO3- reabsorption
What impact does ECF volume have on filtered HCO3-?
Expansion of ECF volume -> decreased HCO3- reabsorption
Contraction of ECF volume -> increased HCO3- reabsorption (contraction alkalosis)
What impact does Angiotensin II have on filtered HCO3-?
Angiotensin II stimulates Na+ - H+ exchange (proximal tubule) and increases HCO3- reabsorption. Contraction alkalosis
Metabolic Acidosis
Over-production or ingestion of fixed acid or loss of base (lower HCO3-) produces & increase in arterial [H+] (acidemia)
Primary disturbance = decreased [HCO3-]
HCO3 is used to buffer the extra acid
What is the primary disturbance of metabolic acidosis?
Lower [HCO3-]
Compensation mechanism for Metabolic acidosis?
Respiratory compensation = hyperventilation (kussmaul breathing; deep rapid respiration, common in type 1 diabetics due to keto acids)
Renal compensation = increased excretion of H as titratable acid & NH4. increase “new” HCO3 reabsorption
Chronic metabolic acidosis = adaptive increase in NH3 synthesis
Metabolic Alkalosis
- Loss of fixed H or gain of base => decrease arterial H (alkalemia)
- Primary disturbance = increase [HCO3-]. eg: vomiting
Compensation for Metabolic Alkalosis
Respiratory Compensation = hypoventilation
Renal compensation = increased HCO3 excretion
What happens if the ECF volume contracts w/ Metabolic Alkalosis?
If ECF volume contraction occurs, HCO3 reabsorption will increase, worsening the metabolic alkalosis
Respiratory Acidosis
Due to decreased respiratory rate & retention of CO2
Primary disturbance = increased arterial CO2 -> increased [H]
What is the primary disturbance of Respiratory Acidosis?
Increase arterial CO2 -> increased [H]
Compensation mechanism for Respiratory Acidosis
No respiratory compensation**; the lungs cannot compensate for themselves
Renal compensation: increased excretion of H as titratable H & NH4. Increased reabsorption of “new” HCO3
Acute vs Chronic Respiratory Acidosis
Renal compensation has not yet occurred w/ acute. Renal compensation occurs w/ chronic.
Respiratory Alkalosis
Due to increased respiratory rate (hyperventilation)
Primary disturbance = decreased PCO2
What is the primary disturbance of Respiratory Alkalosis?
Decreased PCO2
Compensation mechanism for Respiratory Alkalosis
No respiratory compensation
Renal compensation: decrease H+ excretion, increase HCO3 excretion
Acute vs Chronic Respiratory Alkalosis
In acute renal compensation has not yet occurred. In chronic renal compensation is present.