Metabolic acidosis

1. METABOLIC ACIDOSIS
Presenter - Razi Shahid
Date: 29/10/2020
Total no. of slides:
1

2. Learning objectives
Definition of Metabolic Acidosis
Cause
Calculation
Anion Gap
Delta Ratio
Osmolar Gap
Compensation
Respiratory 2

3. Refrences
SOURCE - ACID BASE DISORDERS IN CRITICAL CARE – PART 1 & 2
ANAESTHESIA TUTORIAL OF THE WEEK 66
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e-in-critical-care---part-1.pdf
● chrome-extension://ohfgljdgelakfkefopgklcohadegdpjf/https://www.wfsa
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dc9f668ae9-68-Acid-Base-Disorders-in-Critical-Care---part-2-.pdf
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4. Definition
Metabolic acidosis exists when there is an excess level of fixed or exogenous acids in the
blood.
Fixed acids include hydrochloric acid , ketoacids and lactic acid.
This is always accompanied by a drop in plasma bicarbonate concentration (relative to the
bicarbonate concentration present prior to the onset of the acidosis).
Blood pH will only fall when the buffering capacity of the blood becomes beyond it’s
limitation.
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5. Causes
● Pathophysiological mechanism:
○ (i) A gain of strong acid - Endogenous and Exogenous
○ (ii) A loss of base - Bowel & Kidneys
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6. Classification of Metabolic Acidosis
Based on Calculation
● Anion gap
● Delta ratio
● The size of the Osmolar gap
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7. Anion gap
The anion gap is defined as the concentration difference between the major (measured)
cations and anions within the plasma and is normally 12 to 18 mmol/l.
Anionic proteins, phosphate, sulphate and low levels of organic acids, which are not
measured, account for the difference (i.e. the ‘gap’).
Anion gap = [Na+ K] - [HCO3 + Cl] = 15 (±3) mmol/l
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8. Causes of Normal Anion Gap
• Plasma bicarbonate is low (the hallmark of acidosis) and chloride
concentration is raised.
• This bicarbonate loss may be:
Gastrointestinal (diarrhoea, fistula)
Renal (renal tubular acidosis, drug effect).
• Also occurs with rapid intravenous infusion of normal saline (excess chloride)
or infusions of parenteral nutrition rich in cationic amino acids (e.g. arginine).
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9. Causes of Increased anion gap
Plasma bicarbonate is low and chloride concentration is normal.
Fixed acids may be retained in:
1. Uraemia
2. Ketoacidosis (diabetic, alcoholic)
3. Lactic acidosis.
If fixed acids are normal, exogenous acids should be considered:
1. Salicylate poisoning
2. Methanol poisoning
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10. Delta Ratio
Delta ratio = [Rise in anion gap]
[Drop in bicarbonate]
● In an increased anion gap acidosis every molecule of fixed acid that dissociates in
blood will create one hydrogen ion and one acid anion.
● The H+ will bind one molecule of bicarbonate (buffering), resulting in a drop in
bicarbonate of one for each rise in the anion gap of one.
● The delta ratio for an increased anion gap acidosis will consequently approach one.
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11. Delta Ratio
1. If the delta ratio is very low (less than 0.4) then it is normal anion gap acidosis.
2. If the delta ratio is high (greater than 2) then it is suggested as compensated
respiratory acidosis.
3. A ratio between 0.4 and 2.0 suggests a mixed picture.
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12. Limitations of the Anion Gap and Delta Ratio
● The normal range is quoted as 12 to 18 mmol/l
● It is possible for a patient with a normal anion gap of 12 to acquire a severe lactic
acidosis (plasma lactate greater than 5 mmol/l) with in the normal range.
● The anion gap is also affected by plasma albumin (an important unmeasured anion)
and low albumin levels can significantly offset the rise in anion gap.
● Bicarbonate only accounts for 60% of the buffering capacity of blood and this affects
binding one molecule of H+.
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13. Osmolar Gap
● The osmolar gap represents the difference between a sample’s measured osmolality
and its calculated osmolarity.
● It is a useful calculation to perform if alcohol poisoning.
● Calculated Osmolarity = 2 [Na+] + urea + glucose
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14. Compensation for Metabolic Acidosis
● The body regulates the acidity of the blood by bicarbonate buffering system
● Intracellular buffering is by absorption of H+ atoms by various molecules, including
proteins, phosphates and carbonate in bone.
● Respiratory compensation by hyperventilation.
● Kidney: Renal generation of new bicarbonate due to increase in ammonium
excretion.
● Liver: Hepatic metabolism of acid anions to produce bicarbonate.
● Exogenous Administration of sodium bicarbonate.
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15. Compensation for Metabolic Acidosis
● Buffering provides the main means of accommodating a metabolic acidosis.
● As buffering capacity is exceeded, acidaemia develops.
● Once the rise in hydrogen ion concentration has reached the CSF it is detected by
chemoreceptors and compensation occurs by reducing CO2 levels through
hyperventilation (first described by Kussmaul).
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16. Respiratory changes in metabolic acidosis
● Oxyhaemoglobin dissociation curve (ODC) shifts to the right – due to the acidosis
occurs rapidly.
● Patients with severe metabolic acidosis (diabetic ketoacidosis) generates
hyperventilation (Kussmaul respirations) with minute volumes (20-30 l/min) and
drop pCO2 to below 2 kPa.
● If they are ventilated with a minute volume of 5 l/min then their acidosis will
deteriorate profoundly.
● Because if patient is ventilated with a normal minute volume then the pCO2 level
will rise rapidly towards normal, and acidaemia will worsen, and the patient will
become acutely unstable.
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17. Cardiovascular Changes
● Depression of myocardial contractility
● Sympathetic overactivity
● Resistance to the effects of catecholamines
● Peripheral arteriolar vasodilation
● Venoconstriction of peripheral veins
● Vasoconstriction of pulmonary arteries (increased PAP)
● Hyperkalaemia
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18. Causes of Metabolic Acidosis
● Lactic Acidosis
● Ketoacidosis
● Renal Tube Acidosis
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19. Lactic Acidosis
● Typte1 hypoxia+peripheral generation of Lactate in patient with circulatory
failure+shock.
● Type2 impaired metabolism of Lactate in Liver disease and drug+toxin inhibit lactate
metabolism( eg:metformin)
● >2mmol/l(20mg/dl)
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20. Ketoacidosis
Ketone bodies include β-hydroxybutyrate, acetoacetate and acetone.It is produced when
lipids are metabolised by β oxidation.
The main causes of ketoacidosis include
● Starvation ketoacidosis
● Alcoholic ketoacidosis
● Diabetic ketoacidosis
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21. Renal tubular acidosis
Renal tubular acidosis (RTA) is subdivided according the site of the tubular defect
Type 1 : Distal tubular defect
Type 2 : Proximal tubular defect
Type 4 : Distal tubular resistance to aldosterone (or aldosterone deficiency)
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22. Sign & Symptoms
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23. Approach to Management of Metabolic Acidosis
● History taking.
● Monitoring- GCS, Pulse , Blood Pressure, Respiratory Rate, Temperature, ECG,
Urine Output, ETCo2.
● Emergency:Intubation and ventilation for airway or ventilatory control;
cardiopulmonary resuscitation; severe hyperkalemia
● Cause: Treat the underlying disorder as the primary therapeutic goal.
● Consequently,accurate diagnosis of the cause of the metabolic acidosis is very
important.
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24. Investigation
● ABG
● Urine tests for glucose and ketones
● Electrolytes (incl chloride, anion gap,bicarbonate’)
● Plasma glucose
● Urea and creatinine
● Lactate
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25. Approach to Management of Metabolic Acidosis
● A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may be
treated with intravenous bicarbonate.
● Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the
arterial blood gas readings.
● If the acidosis is particularly severe and/or there may be intoxication, consultation
with the nephrology team is considered useful, as dialysis may clear both the
intoxication and the acidosis.
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26. Approach to Management of Metabolic Acidosis
When treating patients with shock & ketoacidosis , the following points must be
considered and closely monitored:
● Correction of fluid loss with intravenous fluids
● Correction of hyperglycemia with insulin
● Correction of electrolyte disturbances, particularly potassium loss
● Correction of acid-base balance
● Treatment of concurrent infection, if present
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27. Treatment of Type 1 and Type 2 RTA
● Relatively simple, requiring the use of sodium bicarbonate or the slightly more
palatable compound Shohl solution (or Bicitra), which contains citric acid and
sodium citrate, providing 1 mEq/mL of alkali.
● Polycitra K solutions contain potassium citrate to provide 2 mEq/mL of alkali and
2 mEq/mL of potassium,designed to correct both the acidosis and hypokalemia.
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28. Treatment of RTA Type 4
● With fludrocortisone 0.1 to 0.3 mg/d (0.05 to 0.15 mg/m 2 per day).
● To reverse the hyperkalemia that characterizes the metabolic acidosis of type
4 RTA, dietary potassium restriction and orally administered potassium
binders may be needed.
● Finally, to increase renal excretion of potassium, chlorothiazide and
furosemide may be required to correct hyperkalemia. To neutralize the
metabolic acidosis, bicarbonate therapy of 1.5 to 2.0 mEq/kg per day has
been advocated.
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29. Take Home Message
● pH close to 7.1
● Bicarbonate reduction is the hallmark of metabolic acidosis.
● pCo2 increase
● Potassium Increase
● Lactate More than 2mmol/L
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30. Question & Answers
Case 1.
A known diabetic patient presented with severe diabetic ketoacidosis. He was drowsy,
exhibited classical Kussmaul respiration and proceeded to have a respiratory arrest whilst
being admitted to ICU. After immediate intubation the trainee ventilated the patient with
the ventilator’s default settings (rate 12, tidal volume 500ml, PEEP 5cmH2O FiO2 50%)
and attempted to secure arterial and central venous access.Shortly after intubation the
patient became asystolic and could not be resuscitated.
Why did this patient have a respiratory arrest?
Why did he deteriorate after intubation?
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31. Explanation
In this case the patient presented with a metabolic acidosis caused by loss of diabetic
control, relative insulin deficiency and consequently ketoacidosis. (This will be covered in
more detail in part B of the tutorial).
Kussmaul respiration implies respiratory compensation through hyperventilation. The rise
in minute volume can be substantial and maintaining this compensation is very strenuous.
As time passes patients tire, the minute volume decreases and the acidosis worsens rapidly.
Young patients in particular can maintain full respiratory compensation almost to the point
of respiratory arrest, as in this example. Elderly patients tend to tire more slowly and this
allows timely recognition and support.
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32. Explanation
When taking over a patient’s ventilation, in the setting of a metabolic acidosis, it is vital
that the minute volume used is raised appropriately. If standard ventilation settings are
applies, as in this case example, the drop in alveolar ventilation post- induction will
remove the respiratory compensation and the acidosis will deteriorate dramatically.
This is likely to be the cause of this patient’s cardiovascular collapse.
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33. CASE 2
A young woman was admitted to the surgical ward with a history of severe vomiting and
increasing right iliac fossa abdominal pain. On examination she was found to have a rigid
abdomen, with visible subdiaphragmatic gas on CXR.
She was cardiovascularly unstable and her admission bloods showed Hb 17.4, WCC 24.6,
Plateletsts 79, Na+ 125, K+ 4.3,, Cl 93, urea 20.4, creatine 310mcmol/l
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34. ABG
• pH 7.1
• pCO2 5.2kPa
• pO2 29.3 kPa
• HCO3- 14.3
What is the likely cause of her acidosis?
How do you interpret her chloride level?
Is her compensation adequate/maximal?
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35. Explanation
The clinical presentation is of an acute abdomen in a previously fit patient. The raised
haemoglobin, urea and creatinine suggest that the patient is dehydrated and this raises the
possibility of an associated lactic acidosis due to inadequate tissue perfusion. The arterial
gasses confirm that acidaemia is present (low pH) and the low bicarbonate implies that the
acidosis is metabolic.
The anion gap is raised at 35 and this strongly suggests the presence of an increased anion
gap acidosis.
The delta ratio is calculated then this is raised at 3.5 and this suggests a pre-existing
metabolic alkalosis. While it is impossible to be absolutely sure this would seem to fit
clinically.
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36. Explanation
The vomiting that occurred in the days leading up to admission may have caused a
metabolic alkalosis (loss of hydrogen ions and chloride) that was confounded by a
superimposed lactic acidosis on admission. This would also explain why a severe increased
anion gap acidosis only dropped the pH to 7.1 in this example, when you would expect the
pH to be lower.
The vomiting that occurred in the days leading up to admission may have caused a
metabolic alkalosis (loss of hydrogen ions and chloride) that was confounded by a
superimposed lactic acidosis on admission. This would also explain why a severe increased
anion gap acidosis only dropped the pH to 7.1 in this example, when you would expect the
pH to be lower.
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37. CASE 3
An elderly lady was admitted from a care home with a week long history of severe
diarrhoea. She was dehydrated and hypotensive. Admission bloods revealed Na+ 134, K
2.5, Cl 122, Urea 15.4, creatine 280, and ABG
pH - 7.21
pCO2- 2.9kPa
pO2 - 19.5 kPa
HCO3- 6.4
Describe the acid base disorder present. What is the likely aetiology? Is her compensation
adequate?
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38. Explanation
This lady presented with a low pH on arterial gases and low bicarbonate – this implies that
a metabolic acidosis is present. The extent of the dehydration raises the possibility of a
lactic acidosis however this would create an increased anion gap.
The anion gap in this instance is low (8.5) and the delta ratio is 0.5. This strongly supports
the presence of a normal anion gap acidosis secondary to bicarbonate loss from the gut.
With a bicarbonate of 6.4 you would expect the patient to drop her pCO2 in this instance
her respiratory compensation is appropriate. to 2.28 and in this instance her respiratory
compensation is appropriate.
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