Lect 11 Flashcards
What are the three lines of defense against acid/base disturbances
- buffers
- mainly HCO3-/H2CO3; very fast
- respiratory compensation
- adjusts CO2 levels
- very fast but incomplete
- renal compensation
- adjusts HCO3- levels
- slow but potent
which compensation is always active when primary problem is metabolic
respiratory compensation
which compensation will compensate for respiratory problems and metabolic problems if they do not involve the kidney
reanl compensation
Problem
- pH= 7.52
- HCO3- = 22
- PCO2 = 28
- alkalosis
- there is a respiratory component: (PCO2 <35)
- expected HCO3- = 22 (since PCO2 is 12 mmHg below normal which will depress HCO3- by 2 due to mass action)
- actual HCO3- = 22, so there is no renal compensation
- this is an uncompensated (pure) respiratory alkalosis
Problem
- pH = 7.43
- HCO3- = 18
- PCO2 = 28
- normal pH
- primary disturbance is respiratory
- expect HCO3- = 22, but it = 18; therefore, 4 was removed by kidneys
- completely componsated respiratory alkalosis
problem
- pH=7.25
- HCO3- = 12
- PCO2 = 28
- pH = acidosis
- expected HCO3- = 22, but it =12; therefore must be a primary metabolic acidosis that reduced HCO3- by 10
- partly compensated metabolic acidosis
Problem
- pH = 7.30
- HCO3- = 25
- PCO2 = 52
- acidosis
- there is a respiratory acidosis
- expected HCO3- = 25, which it is
- uncompensated (pure) respiratory acidosis
H+ loss or HCO3- gain is consistent with
metabolic alkalosis
Hyperaldosteronism and ECF volume contraction can lead to what condition
- metabolic alkalosis
how can ECF volume contraction due to vomiting or extensive use of diuretics maintain metabolic alkalosis?
- increase in renin-angiotensin II-aldosterone system
- angiotensin II stimulates Na+-H+ antiporter and HCO3- reabsorption
- aldosterone stimulates secretion of H+ (H+-ATPase) from type A intercalated cells and K+ from principle cells
metabolic alkalsosis is often linked with what
hypokalemia
- volume contraction stimulates aldosterone which intensifies both alkalosis and hypokalemia
hypokalemia has what effect on H+ secretion
- stimulates H+ secretion by type A intercalated cells (H+/K+ ATPase) and can increase NH4+ secretion, both intensify alkalosis
metabolic alkalsos can present with hypochloremia. why?
- due to loss in gastric fluids or urine (diuretics)
- without Cl- available for co-transport with Na+, the collecting duct lumen develops a more negative potential with respect to the cytoplasms which facilitates the excretion of K+ and H+
how is metabolic alkalosis treated
- repletion of Cl- deficit with saline (NaCl or KCl)
- corrects saline-responsive forms
- will adjust the RAAS system
- Cl- transport with Na+ reduces negativity of CD lumen, H+ and K+ loss reduced
- result in excretion of bicarbonate
aldosterone excess (secreting tumor) is an example of saline-resistant metabolic alkalosis. What is the treatment
- ECF volume is increased, and [Cl-] is okay
- administering saline does not help as patient is already volume expanded
- excess aldosterone increases H+ secretion and Na+ reabsorption
- treatment: remove tumor or aldosterone antagonist (spironolactone)
a gain of H+ or loss of HCO3- causes
metabolic acidosis
what are the three types of metabolic acidosis from diminished tubular H+ secretion
- type I (distal)
- H+-ATPase activity is reduced
- type II (proximal)
- Na+-H+ antiporter is reduced
- type IV
- reduced formation of NH4+
- often due to hyperkalemia secondary to aldosterone deficiency
- reduced formation of NH4+
what is a anion gap? what is the normal value?
- in the body, the concentration of anions must equal the concentration of cations
- major anions: Cl = 100; HCO3- = 24; total = 124
- major cation: Na+ =140
- anion gap = [Na+] -([Cl-] +[HCO3-])
- normal gap = 8-16
the anion gap often increases in what state? why?
- increases in acidosis where there is an excess of other non-volatile (fixed) acids
- AG is often nml is acidosis due to simple bicarb loss due to Cl- increase
- fixed acids liberate H+ which is buffered by HCO3- w/o changing Cl- levels, this increases the anion gap
- **anions associated with these acids (lactate, oxalate) take the place of HCO3-; so Cl- levels do not change
name some clinical causes of increased anion gap
- lactic acidosis: due to lactic acid
- ketoacidosis: acetoacetic acid
- renal failure: accumulation of phosphoric, sulfuric acid
- salicylate poisoning
high altitude, anxiety, and hypoxemia can cause what state
- respiratory alkalosis
- due to decrease in PaCO2 via increases alveolar ventilation
impairment of central respiratory regulation, chest wall dysfunction, impaired airway mechanisms can cause what state
- respiratory acidosis
- due to impaired pulmonary excretion of CO2
