Acid-Base Disorders 2 (Metabolic Acidosis) Flashcards
Remarks on renal response to pulmonary acid-base disturbances
The renal response to pulmonary acid-base disturbances begins within 30 minutes of onset, but requires hours to days to achieve equilibrium
delta gap
Refers to the relative change in the anion gap (AG)
May be more important than the actual AG value
Virtually all AG values above _____ can be considered abnormal
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
Delta ratio
∆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
Albumin and metabolic acidosis
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
What 2 parameters of blood gas results are the ones that are actually measured (and not just calculated)?
pH and PCO2
HCO3 is calculated via the Henderson-Hasselbalch equation
Respiratory compensation in metabolic acidosis
- With normal respiratory compensation, PCO2 decreases by 1 mm Hg for every net decrease in HCO3
- In a maximally-compensated metabolic acidosis (which takes about 12-24 hours), Winter’s formula applies:
Expected PaCO2 = [(1.5 x HCO3) +8] +/- 2
Limits to the respiratory compensation for metabolic acidosis
- Minute ventilation actually declines when pH decreases below 7.10
- The development of metabolic acidosis that drives the pH below 7.10 is likely associated with a very high risk of inadequate ventilation response
- Administration of HCO3 in the presence of hypoventilation may exacerbate respiratory acidosis, because the HCO3 is converted to CO2 and water
The lowest PCO2 achievable is approximately
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
The differential diagnoses for HAGMA in emergency practice fall into 4 broad categories, namely
Renal failure
Ketoacidosis
Lactic acidosis
Ingestions
The major ketone present in the serum of a patient with untreated diabetic or alcoholic ketoacidosis may be
B-hydroxybutyrate
Remarks on lactic acidosis
Lactic acidosis is not a diagnosis, but a syndrome with its own differential diagnosis.
Remarks on ethanol
Ethanol should never be considered the cause of an significant metabolic acidosis.
Look for other causes
Triple acid-base disturbance
- HAGMA
- Metabolic alkalosis
- 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]
Treatment of metabolic acidosis
- The treatment of metabolic acidosis reflects the treatment of the underlying disorder and the restoration of normal tissue perfusion and oxygenation 🔸
- 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.
- If there is inadequate respiratory compensation, the appropriate treatment will be to first correct the respiratory problem 🔸