Arterial Blood Gases Flashcards
Which are the primary four acid-base disorders?
- Respiratory acidosis
- Metabolic acidosis
- Respiratory alkalosis
- Metabolic alkalosis
What are the three mechanisms by which the body controls the blood’s acid-base balance within this narrow range?
- Intracellular & extracellular buffers
- Regulation by the kidneys
- Regulation by the lungs
How do lungs and kidneys regulate the pH?
Lungs
- Regulate the pCO2 by adjusting the rate of alveolar ventilation
Kidneys
- Regulate the [HCO3-] by adjusting the renal excretion of carbonic acid and the reabsorption of bicarbonate
What is base excess?
The base excess is the quantity of base or acid needed to titrate one litre of blood to pH 7.4 with the pCO2 held constant at 5.3 kPa
- In the context of an acidosis a negative base excess indicates there is a metabolic component
What are the five steps to interpreting ABG results?
- Is there an acidaemia or an alkalemia?
- Is the primary disturbance respiratory or metabolic?
- For a metabolic acidosis, is there a high anion gap?
- Is there compensation? If there is, is it appropriate?
- What is the alveolar-arterial gradient? Look at the arterial pO2 in the context of the inspired oxygen concentration and the arterial pCO2.
What is the anion gap and how is it calculated?
In the body, the # of cations and anions are equal
- Blood tests measure mostly cations but only a few anions
- Adding all the measured anions & cations together leaves a gap that reflects unmeasured anions (e.g. plasma protein albumin)
Calculated as follows
- Na+ - (HCO3- + Cl-)
- The normal AG is 8-16 mmol/l
- If K+ is included, the normal range is 12-20 mmol/l
- Of the 8-16 mmol/l anion gap, 11 mmol/l is typically due to albumin
- Reduction in albumin > reduce the baseline anion gap
- The AG is reduced by ~ 2.5 mmol/l for every 10 g/l fall in [Albumin]
Main causes of a high anion gap acidosis (> 16 mmol/l)
- Increased endogenous acid production
- Ketoacidosis (e.g. alcohol, starvation, diabetes)
- Lactic acidosis
- Type A: Tissue oxygenation impaired
- Increased lactate from anaerobic tissue metabolism in states of hypoperfusion, e.g. shock
- Type B: Tissue oxygenation not impaired
- E.g. reduced lactate metabolism in liver
- Type A: Tissue oxygenation impaired
- Lactic acidosis
- Ketoacidosis (e.g. alcohol, starvation, diabetes)
- Increased exogenous acids
- Methanol
- Ethylene glycol (antifreeze)
- Aspirin
- Inability to excrete acid
- Chronic renal failure
Main causes of acidosis with a normal anion gap (8-16 mmol/l)?
- Loss of bicarbonate
- GI tract
- Diarrhoea
- Ileostomy
- Pancreatic, biliary, intestinal fistula
- Renal
- Type 2 (proximal) renal tubular acidosis
- Carbonic anhydrase inhibitors
- GI tract
- Impaired renal acid excretion
- Type 1 (distal) renal tubular acidosis
- Type 4 renal tubular acidosis (hypoaldosteronism)
How to correct the anion gap for patients with a low albumin concentration?
First, calculate the anion gap: Na - (HCO3 + Cl)
- 135 - (20 + 100) = 15 mmol/l (within the normal range of 8-16)
Then, correct the anion gap for the low albumin
- Anion gap = 15 mmol/l
- Albumin = 20 (n=40) > reduced by 20 g/l
- For every 10g/l fall in albumin > AG reduced by ~ 2.5 mmol/l
- Therefore, the AG was reduced by 5 mmol/l
- When you correct it, the anion gap is 15 + 5 = 20 mmol/l
Is there a compensation?
Compensation refers to the action taken by the body to restore the correct acid-base balance. The normal compensatory measures are:
- Buffers (haemoglobin, plasma proteins, bicarbonate, and phosphate) (minutes)
- Ventilatory response (minutes to hours)
- Renal response (up to several days (3-5))
The compensation is always in the same direction as the initial chemical change
- The basis of compensatory responses is to maintain the HCO3:pCO2 ratio
- Remember the Henderson-Hasselbalch relationship
-
pH ~ HCO3 / pCO2
*
-
pH ~ HCO3 / pCO2
- Remember the Henderson-Hasselbalch relationship
Summary of compensatory responses
Respiratory acidosis
- ^ pCO2 >> ^ HCO3
- Magnitude of compensation
- For every 1.3 kPa ^pCO2 above 5.3 kPa in acute respiratory acidosis
- The HCO3 increases by 1.0 mmol/l
- The pH decreases by 0.07
- For every 1.3 kPa increase in pCO2 above 5.3 kPa in chronic respiratory acidosis
- The HCO3 increases by 3.5 mmol/l
- The pH decreases by 0.03
- For every 1.3 kPa ^pCO2 above 5.3 kPa in acute respiratory acidosis
Respiratory alkalosis
- Reduced pCO2 >> Reduced HCO3
- For every 1.3 kPa decrease in pCO2 below 5.3 kPa in acute respiratory alkalosis:
- The HCO3 decreases by 2.0 mmol/l
- The pH increases by 0.08
- For every 1.3 kPa decrease in pCO2 below 5.3 kPa in chronic respiratory alkalosis
- The HCO3 decreases by 5.0 mmol/l
- The pH increases by 0.03
- For every 1.3 kPa decrease in pCO2 below 5.3 kPa in acute respiratory alkalosis:
Compensatory responses for metabolic disorders are not as predictable as those that occur for respiratory disorders
Metabolic compensation
Metabolic compensation takes days, occurs in two steps
- Min - hours - Cellular buffering (elevates [HCO3] only slightly)
- 3-5 days - Renal compensation
In respiratory acidosis
- Renal excretion of carbonic acid & reabsorption of bicarbonate is increased
In respiratory alkalosis
- The kidneys compensate by reducing reabsorption of bicarbonate and excretion of carbonic acid
Respiratory compensation
Respiratory compensation takes hours
- Max resp compensation for a metabolic disorder takes 12-24 hours (begins in the first hour)
Metabolic acidosis
- Stimulation of the central & peripheral chemoreceptors that control respiration >> increase in alveolar ventilation >> compensatory respiratory alkalosis
Metabolic alkalosis
- Difficult to hypoventilate to compensate
- The resp system rarely retains pCO2 above 7.5 kPa
- A value greater than this suggests a mixed disorder - metabolic alkalosis and resp acidosis rather than compensated metabolic alkalosis
Mixed acid-base disorders
Consider Mixed acid-base disorder when:
- The compensatory response occurs but the level of compensation is inadequate or too extreme
- The pCO2 & [HCO3] become abnormal in the opposite direction (one elevated, one reduced)
- In simple AB disorders, the direction of compensatory response is always the same as that of the initial abnormal change
- The pH is normal, but pCO2 or [HCO3] abnormal
- In simple AB disorders, the compensatory responses rarely return the pH to normal
- If this happens, suspect a mixed disorder
A rule of thumb for mixed acid-base disorders
- When pCO2 is elevated and [HCO3] reduced
- Respiratory acidosis & metabolic acidosis coexist
- When pCO2 reduced and [HCO3] elevated
- Respiratory alkalosis & metabolic alkalosis coexist
