Metabolic acidosis and alkalosis Flashcards
1
Q
Overview of acidemia and alkalemia
A
- Decrease in HCO3- is metabolic acidosis
- Increase in PCO2 is respiratory acidosis
- Increase in HCO3- is metabolic alkalosis
- Decrease in PCO2 is respiratory alkalosis
2
Q
Compensatory mechanisms
A
- Metabolic acidosis (decrease in HCO3-) is compensated by respiratory alkalosis (decrease in PCO2 means increasing RR, so you get hyperventilated in met acidosis)
- Likewise, respiratory alkalosis is compensated by metabolic acidosis
- Metabolic alkalosis (increase in HCO3-) is compensated by respiratory acidosis (increase in PCO2 means reducing RR, so you get hypoventilation in met alkalosis)
- Likewise, respiratory acidosis is compensated by metabolic alkalosis
3
Q
Degree of compensation
A
- Compensation is never complete
- Respiratory compensation rapid, renal is slow
- Compensation may or may not be appropriate degree
- Degree is based on how much compensatory change there is per 1 unit change of the primary d/o
- If there is appropriate compensation it is a simple d/o
- If the compensation is not appropriate the d/o is mixed
- Important note: hypoxia will also override a compensation (thus respiratory compensation for metabolic alkalosis is variable b/c can’t hypo ventilate too much)
4
Q
Normal values
A
- pH: 7.35-7.45
- PO2: 75-105mmHg
- PCO2: 33-44mmHg
- HCO3-: 22-28 mEq/L
5
Q
Determining which type of d/o it is 1
A
- First look at pH to determine if its acidosis or alkalosis
- Then look at bicarb to see if its a compensation of primary disturbance
- Then look at PCO2 to see if its compensation or primary disturbance
- If pH is low and bicarb is low its metabolic acidosis (PCO2 will be low- compensation)
- If pH is high and bicarb is low (compensation) its respiratory alkalosis (PCO2 will be low)
6
Q
Determining which type of d/o it is 2
A
- If pH is high and bicarb is high its metabolic alkalosis (PCO2 will be high-compensation)
- If pH is low and bicarb is high (compensation) its respiratory acidosis (PCO2 will be high)
- Whatever the compensation is (either changing PCO2 or HCO3-), it is always in the same direction as the primary d/o but the other component is changing
7
Q
Calculating how appropriate the compensation of metabolic acidosis is
A
- For each 1 mEq/L drop in HCO3-, there should be a 1.2mmHg drop in PCO2
- To do it quickly, compare the PCO2 to the last 2 digits of the pH
- These two numbers should be close to each other (≤3)
- If they are not then the response is not appropriate
- If, for example, the pH is high but both PCO2 and HCO3 are shifted toward alkalemia (PCO2 down and HCO3 up- going in opposite directions) there is no compensation, or it is not appropriate, thus the problem is mixed
8
Q
Metabolic acidosis etiologies
A
- Ingestion of acid: breakdown products of ethylene glycol, methanol, toluene, salicylic acid
- Endogenous generation of acid: lactic acidosis, ketoacidosis (from DM or etoh), rhabdomyolysis
- Defective acid excretion: renal failure, distal renal tubular acidosis
- Loss of alkali: diarrhea, proximal renal tubular acidosis (RTA)
9
Q
Serums anion gap
A
- Represents unmeasured anions - cations difference (mainly due to albumin normally)
- Formula: [Na] - ([Cl] + [HCO3])
- Normal gap is 8-12
- Causes of high anion gap metabolic acidosis: MUDPILES plus rhabdo and toluene
- Workup to differentiate btwn DDxs: serum urea, Cr, glc, CK, ketones, lactate, etoh, salicylate, urine microscopy (crystals = toluene)
10
Q
MUDPILES
A
- DDx for high anion gap
- Methanol
- Uremia
- Diabetic Ketoacidosis
- Paraldehyde
- Iron and isoniazid
- Lactic acidosis
- Ethylene glycol and etoh
- Salicylates
- Also: toluene and rhabdo
11
Q
Serum osmolal gap
A
- Calculated osmolality: 2[Na] + [BUN]/2.8 + [glc]/18
- If this is >10mOsm/kg different from the measured Sosm there is a high osmolal gap
- DDx for high anion and osmolal gap metabolic acidosis: ethanol, ethylene glycol, propylene glycol, methanol
- High osmolal gap but no anion gap: isopropanol
- High anion gap but no osmolal gap: salicylates
12
Q
Non anion gap metabolic acidosis
A
- Diarrhea or renal tubular acidosis
- Hyperchloremic state b/c lose HCO3- and gain Cl- at equal rate so no gap forms
13
Q
Renal tubular acidosis (RTA)
A
- Failure of kidneys to excrete acids
- RTA is selective defect in tubule acid/bicarb handling
- Renal failure is decrease in # of functioning nephrons
- 3 types of RTA: proximal and (type 2) distal (distal further broken into type 1 and type 4)
14
Q
Types of RTA
A
- Type 2: can’t reabsorb HCO3 in PT, can be due to MM, heavy metals (wilson’s) Rx with high levels of NaHCO3
- Type 1: distal tubule can’t secrete H+ thus can’t form NH4+, can be due to autoimmune (SLE, sjogrens), cirrhosis, amphotericin Rx w/ low NaHCO3
- Type 4: not enough NH4+ excretion due to hypoaldosteronism-> hyperkalemia (also hyporeninemic), can be from DM, SCD, obstruction Rx w/ low K diet and diuretics
15
Q
Clinical features of RTA
A
- Urine NH4+ and HCO3- are both high in type 2 and both low in type 1 and 4
- Urine pH is >5.5 in type 2 and type 1 (type 1 pH should be higher than type 2) and <5.5 in type 4
- Serum K is low in type 2 and 1 and high in type 4
