Acid base disorders Flashcards

1
Q

Difference between respiratory and metabolic disturbances.

A

respiratory acidosis: ↑ CO2
respiratory alkalosis: ↓ CO2

Metabolic acidosis: ↓ HCO3-
Metabolic alkalosis: ↑ HCO3-

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2
Q

What direction is compensation?

A

It is always in the same direction as the primary change and with the corresponding molecule.

Ie: respiratory alkalosis initial change = ↓ PCO2
- compensation is ↓ [HCO3-]

Ie: Metabolic alkalosis initial change = ↑ [HCO3-]
- compensation is ↑ [CO2]

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3
Q

In acute respiratory alkalosis, the HCO3- is expected to fall by _____ meq/l for every ___ fall in PCO2-

A

↓2 HCO3-, ↓ 10 pCO2

2:10

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4
Q

In chronic respiratory alkalosis, the HCO3- is expected to fall by _____ meq/l for every ___ fall in PCO2-

A

↓4 HCO3-, ↓ 10 pCO2

4:10

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5
Q

During respiratory alkalosis, how is compensation with ↓ HCO3 achieved?

A
  1. cell H+ release (acute)
  2. renal H+ retention (chronic)
  • either way, H+ binds to HCO3- which lowers it and drives CO2 formation
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6
Q

During respiratory acidosis, how is compensation with ↑ HCO3- achieved?

A
  1. cell buffering (acute)

2. Renal H+ EXCRETION (HCO3- resorption) (Chronic)

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7
Q

In acute respiratory ACIDOSIS, the HCO3- is expected to INCREASE by _____ meq/l for every ___ INCREASE in PCO2-

A

↑ 1 HCO3-, ↑10 pCO2

1:10

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8
Q

In chronic respiratory ACIDOSIS, the HCO3- is expected to INCREASE by _____ meq/l for every ___ INCREASE in PCO2-

A

↑ 4 HCO3-, ↑10 pCO2

4:10

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9
Q

Metabolic alkalosis requires generation and maintainance,

How does generation of met alk occur?

A
  1. addition of HCO3-
  2. loss of H+
  3. Loss of Cl- rich fluids (contraction alkalosis)
  4. post hypercapnea
  5. hypokalemia
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10
Q

Ways that loss of H+ can occur leading to metabolic alkalosis?

A
  1. GI loss
  2. Renal loss: loop/thiazide diuretics, mc excess
    - inhibit N+ resorption→ increase Na+ delivery to distal tubule → resorbs Na+ → generates (-) charged tubular lumen → FAVORS H+ SECRETION →metabolic alkalosis
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11
Q

maintenance of metabolic alkalosis is ALWAYS due to what?

A

the inability to excrete excess HCO3-

met alk is due to primary increase in HCO3-

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12
Q

How does chloride depletion result in maintaining met alk?

A

it results in the resorption of HCO3- via Cl-/HCO3- exchanger on basolateral mem.

  • note that Cl- depletion is frequently accompanied by volume depletion
    (remember that maintenance of met alk is always due to inability to excrete excess HCO3-)
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13
Q

Why does increased mineralocorticoid activity result in maintaining met alk?

A

They stim the H+-ATPase pump leading to secretion of H+ into the lumen.
This is accompanied by bicarb resorption.

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14
Q

Aldosterone and mineralocorticoids effects on H+-ATPase activity. What significance does this have on metabolic disturbances?

A

Increase H+-ATPase pump, eventually reabsorbing HCO3- and maintaining metabolic alkalosis

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15
Q

Metabolic alkalosis is divided into 2 categories:

A
chloride responsive (saline responsive)
- UCl 20 meq/L
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16
Q

causes of Cl- resistant metabolic alkalosis

A

Excess mineralocorticoids:

  • hyperaldosteronism
  • cushing syndrome
17
Q

Treatment of metabolic alkalosis is urgent bc?

A

urgent bc:

  1. cardiac arrythmias
    - increases sensitivity to catecholamines
  2. hypocalcemia
18
Q

tx for metabolic alkalosis

A
  • mechanical ventilation
  • if Cl responsive: infusion of NaCl/KCl
  • If Cl resistant: block mineralocorticoid effect with spirinolactone or amiloride