Acid-Base Disorders 2 (Metabolic Acidosis) Flashcards

1
Q

Remarks on renal response to pulmonary acid-base disturbances

A

The renal response to pulmonary acid-base disturbances begins within 30 minutes of onset, but requires hours to days to achieve equilibrium

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2
Q

delta gap

A

Refers to the relative change in the anion gap (AG)
May be more important than the actual AG value

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3
Q

Virtually all AG values above _____ can be considered abnormal

A

15 mEq/L, even when there are no previous comparison values available
The common laboratory threshold is 12 mEq/L
Elevations of the AG are most commonly associated with METABOLIC ACIDOSIS

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4
Q

Delta ratio

A

∆AG / ∆HCO3
<0.4 –> Pure NAGMA
0.4 -0.8 –> NAGMA + HAGMA
0.8 - 2.0 –> Pure HAGMA
>2.0 –> HAGMA + met alk (or preexisting compensated resp acid)

normal AG is 12. normal HCO3 is 24

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5
Q

Albumin and metabolic acidosis

A

Hypoalbuminemia may mask the presence of a high AG metabolic acidosis (HAGMA).
For every drop in the albumin level by 1 g/dL, the normal AG range should be lowered by approximately 2.5

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6
Q

What 2 parameters of blood gas results are the ones that are actually measured (and not just calculated)?

A

pH and PCO2
HCO3 is calculated via the Henderson-Hasselbalch equation

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7
Q

Respiratory compensation in metabolic acidosis

A
  1. With normal respiratory compensation, PCO2 decreases by 1 mm Hg for every net decrease in HCO3
  2. In a maximally-compensated metabolic acidosis (which takes about 12-24 hours), Winter’s formula applies:
    Expected PaCO2 = [(1.5 x HCO3) +8] +/- 2
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8
Q

Limits to the respiratory compensation for metabolic acidosis

A
  1. Minute ventilation actually declines when pH decreases below 7.10
  2. The development of metabolic acidosis that drives the pH below 7.10 is likely associated with a very high risk of inadequate ventilation response
  3. Administration of HCO3 in the presence of hypoventilation may exacerbate respiratory acidosis, because the HCO3 is converted to CO2 and water
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9
Q

The lowest PCO2 achievable is approximately

A

12 mm Hg
- This lower limit is obtainable PCO2 is due to resistance in airflow and increased CO2 generated by the exertion required for rapid ventilation, both offsetting the ventilator exhalation of CO2
- the superimposition of respiratory acidosis on a patient in such a condition will result in a RAPID decline of pH to levels at which organ function drops and pharmacotherapy will fail
- noninvasive or mechanical ventilation usually should be instituted in such situations to sure the ventilatory rate and volume are sufficient to prevent an increase in PCO2 at this critical time

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10
Q

The differential diagnoses for HAGMA in emergency practice fall into 4 broad categories, namely

A

Renal failure
Ketoacidosis
Lactic acidosis
Ingestions

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11
Q

The major ketone present in the serum of a patient with untreated diabetic or alcoholic ketoacidosis may be

A

B-hydroxybutyrate

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12
Q

Remarks on lactic acidosis

A

Lactic acidosis is not a diagnosis, but a syndrome with its own differential diagnosis.

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13
Q

Remarks on ethanol

A

Ethanol should never be considered the cause of an significant metabolic acidosis.
Look for other causes

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14
Q

Triple acid-base disturbance

A
  1. HAGMA
  2. Metabolic alkalosis
  3. Respiratory alkalosis
    Seen in sepsis (lactic acidosis) and salycylate poisoning

[But I think this should be Respi alk –> Metab acid –> Respi acid, as seen in sepsis and aspirin toxicity]

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15
Q

Treatment of metabolic acidosis

A
  1. The treatment of metabolic acidosis reflects the treatment of the underlying disorder and the restoration of normal tissue perfusion and oxygenation 🔸
  2. The most important step 🔸 is to determine whether there is a respiratory component to the acidosis (i.e., a primary respiratory acidosis), because the treatment approach differs.
  3. If there is inadequate respiratory compensation, the appropriate treatment will be to first correct the respiratory problem 🔸
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16
Q

Bicarbonate therapy may be appropriate for limited indications

A
  1. Severe hypobicarbonatemia (HCO3 <4 mEq/L)
    - insufficient buffer concentrations may lead to extreme increases in acidemia with small increases in acidosis
  2. Severe acidemia (pH <7.00 to 7.15)
    - in cases of HAGMA with signs of shock or myocardial irritability that has not responsded to supportive measures includeing adequate ventilation and fluid resuscitation
  3. Severe hyperchloremic acidemia
    - lost bicarbonate must be generated by kidneys and liver, which may require days
17
Q

When given, HCO3- can be dosed how?

A
  1. 0.5 mEq/kg for each mEq/L rise in HCO3 desired
  2. the goal is to restore adequate buffer capacity (HCO3 >8 mEq/L) or to achieve clinical improvement in shock or dysrhythmias
  3. Bicarbonate should be given as slowly as the clinical situation permits
  4. 75 mL of 8.4% sodium bicarbonate in 500 mL of D5W produces a nearly isotonic solution for infusion
  5. Adequate time should be allowed for the desired effect to be achieved, with monitoring of acid-base balance