Acid-Base Disorders Flashcards

1
Q

Major types of acid-base disorders

A
  1. Respiratory alkalosis (decrease in CO2 resulting in a increase in pH)
  2. Respiratory acidosis (increase in CO2 resulting in a decrease in pH)
  3. Metabolic alkalosis (increase in HCO3 resulting in an increase in pH)
  4. Metabolic acidosis (decrease in HCO3 resulting in decrease in pH)
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2
Q

Respiratory alkalosis: Definition/differenital dx

A
  • respiratory process caues primary decrease in PCO2
  • DDx:
    • always due to hyperventilation
    • pulmonary disease
    • hypoxemia
    • mechanical ventilation
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3
Q

Respiratory alkalosis: compensation

A
  • decreased HCO3 due to:
    • H+ release from cells (acute)
    • renal H+ retention (chronic)
      • takes 3-5 days to complete
  • compensation rules:
  • ##### Acute: ΔHCO3- = ↓ 2 meq/L for every 10 mmHg ↓ in PCO2 [↓(2:10)]
  • ##### Chronic (3 to 5 days): ΔHCO3- = ↓4 meqL for every 10 mmHg ↓ in PCO2 [↓(4:10)]
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4
Q

Respiratory alkalosis: Signs, Sx, Tx

A
  • Lab abnormalities: decreased potassium (small); decreased phosphorus (may be large).
  • Symptoms: neurologic (paresthesias, carpopedal spasms).
  • Consequences: decreased intracranial pressure, cardiac arrhythmias.
  • Tx: treat underlying cause; can depress ventilation w/sedative
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5
Q

Respiratory acidosis: definition, DDx

A
  • respiratory process causes a primary increase in the PCO2
  • DDx:
    • always due to inadequate respiration @ 4 steps of respiration: sensing/signaling, muscles, free flow, gas exchange
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6
Q

Respiratory acidosis: compensation

A
  • increased HCO3 due to:
    • cell buffering (acute)
      • H+ reabsorbed by intracellular buffers
    • renal H+ excretion (chronic)
      • 3-5 days
  • pH should not fall below 7.20 in appropriately compensated chronic respiratory acidosis
  • compensation rules:
  • Acute: ΔHCO3- = ↑ 1 meq/L for every 10 mmHg ↑ in PCO2 [↑ (1:10)]
  • Chronic (3 to 5 days): ΔHCO3- = ↑4 meqL for every 10 mmHg ↑ in PCO2 [↑ (4:10)]
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7
Q

Respiratory acidosis: Signs, Sx, Tx

A
  • Symptoms: Neurologic: headache, decreased arousal/sleepiness (aka CO2 narcosis)
  • Consequences: Increased intracranial pressure, cardiac arrhythmias, hypotension from peripheral vasodilatation
  • **Treatment: **
    • Treat underlying cause
    • Pay attention to PO2
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8
Q

Metabolic alkalosis: definition, DDx

A
  • metabolic process causes primary increase in HCO3
  • DDx:
    • generation of bicarb increase
      • addition of HCO3
      • loss of H+
      • loss of fluid w/chloride
      • post-hypercapneia
      • hypokalemia
    • maintenance of met alk is always due to renal inability to excrete excess HCO3
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9
Q

Main mechanisms that generate metabolic alkalosis

A
  1. Added HCO3 via:
    1. direct admin of bicarb
    2. direct admin of substrate metabolized to bicarb
  2. Loss of H+ via:
    1. GI loss: vomiting
    2. Renal loss: loop, thiazide diuretics, mineralcorticoid excess
  3. Loss of chloride rich fluid
    1. loop diuretics
    2. cystic fibrosis
  4. post-hypercapnia
    1. metabolic alkalosis in patient w/chronic respiratory acidosis + mechanical ventilation
  5. hypokalemia
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10
Q

Mechanisms of maintenance of metabolic alkalosis

A
  • chloride depletion ==> increased resorption of bicarb (chloride vs. non-chloride responsive met alk)
  • potassium depletion
  • increased mineralocorticoid activity ==> stimulate H+ ATPase to secrete H+ into tubule ==> bicarb resorption
  • hypovolemia ==> release of aldosterone ==> increased Na resorption + bicarb (to maintain electroneurtrality)
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11
Q

Definition/causes of chloride responsive metabolic alkalosis

A
  • [UCl] < 20 mEq/L => chloride depletion is major maintence factor
  • major causes:
    • diuretics
    • vomiting, gastric drainage
    • villous adenomas
    • congenital chloride-losing diarrhea
    • cystic fibrosis
    • post-hypercapnia
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12
Q

Definition/causes of chloride resistant metabolic alkalosis

A
  • [UCl] > 20 mEq/L
  • causes:
    • excess mineralocorticoids
      • hyperaldosteronism
      • cushing’s syndrome
    • licorice ingestion
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13
Q

Metabolic alkalosis: compensation

A
  • rise in pH ==> decrease in ventilation ==> rise in CO2
  • compensation rules:
  • ΔCO2 (in mmHg) = 0.25 – 1.0 XΔHCO3
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14
Q

Metabolic alkalosis: treatment

A
  • possible severe consequences:
    • cardiac arrhythmias
    • hypocalcemia => neuromuscular irrability => tetany
  • hypoventilation via mechanical vent
  • Chloride responsive = Infusions of NaCl or KCl
  • Chloride resistant = block mineralocorticoid effect w/sprionolactone
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15
Q

Metabolic acidosis: definition, DDx

A
  • metabolic process causes primary decrease in HCO3
  • DDx/major mechanisms:
    • loss of bicarbonate = normal anion gap
    • addition of acid = increased anion gap
    • anion gap = [Na] - [Cl] - [HCO3]
      • normal = 9 +/- 3
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16
Q

Characteristics of non-anion gap metabolic acidosis

A
  • caused by loss of bicarb
  • loss of bicarb is replaced by an increase in chloride
17
Q

Characteristics of anion gap metabolic acidosis

A
  • caused by addition of acid ==> decrease in bicarb/loss of anion from plasma
  • anions other than chloride increase to maintain electroneutrality
  • anion gap is “increased” when > 18
18
Q

Causes of non-anion gap metabolic acidosis

A
  • loss of bicarb
  • GI loss: diarrhea
    • urine pH < 5.3
    • urine anion gap < 0
  • renal loss: renal tubular acidosis = due to defect in renal bicarbonate or hydrogen ion handling
    • proximal, distal, hyperkalemic
    • urine pH > 5.3
    • urine anion gap > 0
19
Q

Causes of anion gap metabolic acidosis

A
  • MUD PILES:
  • Methanol
  • Uremia (renal failure)
  • DKA
  • propylene Glycol
  • INH (isoniazid)
  • Lactate
  • Ethylene Glycol
  • Salicylates
20
Q

Physiologic effects of metabolic acidosis

A
  • myocardial contractility decreases + peripheral resistance falls ==>
  • hypotension, pulmonary edema, vfib
  • respirations = deep and rapid (Kussmaul’s)
  • chronic ==> hypercalcuira + bone disease
21
Q

Metabolic acidosis: compensation

A
  • increased ventilation ==> fall in PCO2
    • = incomplete compensation
  • appropriate compensation:
    • Δ PaCO2 (in mmHg) = 1.0 – 1.5 x Δ **[HCO3-] (in mEq/L) **
    • quick approximation: PCO2 = last 2 digits of pH
  • both HCO3 and PCO2 should be decreased; if this does not occur likely a mixed disorder__​
22
Q

Mixed disorder: primary respiratory alkalosis + metabolic acidosis

A
  • Δ PaCO2 (in mmHg) > 1.0 – 1.5 x Δ [HCO3-] (in mEq/L)
23
Q

Metabolic acidosis: Tx

A
  • correct underlying disorder
  • chronic = oral sodium bicarbonate
24
Q

Characteristics of mixed disorders

A
  • coexistence of two+ primary acid-base disorders
  • expected compensation will be less than or greater than expected
  • PCO2 and HCO3 differ from normal in opposite direction