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Acid-base

Up Acid-base Hyponatraemia Lactate Magnesium Phosphate Potassium


Pyroglutamic acidosis

Acid-Base disturbance

Metabolic acidosis

Anion gap = Na-(Cl + HCO3)

Normal anion gap = 3-11 mEq/L. (8-16 if K is included in equation). Made up of unmeasured anions. Consist of proteins, mainly albumin. As a result a reduction of albumin can reduce the baseline anion gap so that a hypoalbuminaemic patient may not have a high anion gap even in the presence of a disorder which usually produces an increased anion gap. Anion gap is reduced by approx 2.5 mEq/L for every 10g/L fall in albumin. Alternatively a corrected value for a a normal anion gap (assuming K is included in calculation of anion gap) can be otained from:

Corrected normal anion gap = 0.2[albumin] x 1.5[phosphate]

where albumin is in g/L and phosphate in mmol/L

Aetiology

Increased anion gap

  • renal failure (late stage)
  • lactic acidosis
    Type A
    - exercise
    - shock
    - severe hypoxia (PaO2<4.7)
    - anaemia
    - post convulsion

    Type B
    Drug induced
    - biguanides eg metformin
    - ethanol, methanol
    - salicylates
    - sorbitol, fructose, xylitol
    - paracetamol poisoning
    Associated with other disease states
    - DM
    - renal failure
    - liver disease
    - infection
    - leukaemia/lymphoma
    - pancreatitis
    - thiamine deficiency
    - short bowel syndrome
    Hereditary
    - glucose-6-phosphatase deficiency
    - hepatic fructose-1,6-diphosphatase deficiency
  • ketoacidosis
    - loss of ketone anions in urine, particularly during IV fluid therapy may attenuate the expansion of the anion gap. During fluid repletion the blood levels of ketoacids diminishes as acetoacetic acid and beta hydroxybutyric acid are excreted in the urine. As a result ketones may be lost in urine before thay can be metabolized back to bicarbonate. Thus loss of ketone anions in urine is tantamount to loss of bicarbonate. Net effect is that high anion gap acidosis present before therapy may be converted into normal anion gap acidosis
    - NB detection of ketonuria by stick testing and of ketonaemia by testing serum dilutions with nitroprusside (Acetest) reagent may be misleading occasionally as these tests only react to acetoacetate and not beta hydroxybutyrate.
  • rhabdomyolysis
  • poisoning: salicylates, methanol, ethylene glycol, paraldehyde, toluene.
    - comparison of measured and calculated osmolality may provide some clue to the presence of methanol or ethylene glycol in the blood. However ethanol may also produce an "osmolal gap" and for unknown reasons moderately elevated "osmolal gaps" (up to 10-15 mOsm/kg) may occur in patients with lactic acidosis or alcoholic ketoacidosis
  • pyroglutamic acidosis

Normal anion gap

  • acid administration eg hyperalimentation with HCl-containing amino acid solutions
  • bicarbonate losses
    - GI: diarrhoea, pancreatic or biliary drainage, urinary diversions
    - renal: type 2 RTA, ketoacidosis (particularly during therapy), post-chronic hypocapnia
  • impaired renal acid excretion
    - with hypokalaemia: classic distal (type 1) RTA
    - with hyperkalaemia: hyperkalaemic distal RTA, hypoaldosteronism (type 4) RTA
    - reduced renal perfusion

Metabolic acidosis and respiratory alkalosis

  • stimulation of respiratory centre by acidaemia causes a fall in PCO2 that in uncomplicated metabolic acidosis can be estimated from:
    Expected PCO2 (mmHg)=1.5xHCO3+ + 8 ±2
  • lower than expected PCO2 indicates a superimposed respiratory alkalosis whereas a higher PCO2 indicates a respiratory acidosis. Equation only useful if plasma bicarbonate <20 mmol/L
  • alternatively: a decrease in PCO2 of 0.16 kPa can be expected for a decrease in bicarbonate of 1 mmol/L. Ideally use nomogram
  • complete respiratory compensation for primary metabolic acidosis does not occur
  • respiratory compensation for acute acidosis tends to be somewhat greater than for chronic metabolic acidosis. Minimum level of PCO2 that can usually be attained is approx 1.3 kPa. Levels <2-2.7 kPa rarely maintained in chronic metabolic acidosis
  • common causes: - salicylate overdose
    - sepsis
    - combined hepatic and renal insufficiency (cirrhosis often associated with chronic respiratory alkalosis)
    - recent alcohol binge (alcoholic ketoacidosis + hyperventilation due to DTs)

Metabolic acidosis and respiratory acidosis

  • may be suspected from the clinical setting: typical acid-base disorder after cardiac arrest or severe pulmonary oedema
  • acidaemia usually very severe
  • if ABGs analysed as a respiratory acidosis the bicarbonate will be found to be lower than appropriate for the level of PCO2. If analysed as a metabolic acidosis the PCO2 will apppear inappropriately high
  • in patients with chronic respiratory acidosis superimposed metabolic acidosis may reduce the bicarbonate only to a level appropriate for an acute respiratory acidosis. Correct diagnosis depends on an analysis of the history and availability of previous acid-base measurements

Metabolic acidosis and alkalosis

  • pH may be normal, alkalaemic or acidaemic depending on the relative magnitude of the primary disorders
  • ABGs are not diagnostic as they can fall within the range expected for either metabolic alkalosis or acidosis or be in the normal range
  • recognition depends largely on the clinical setting and history. Most common cause is metabolic alkalosis due to vomiting superimposed on diabetic or alcoholic ketoacidosis. Ingestion of large amounts of absorbable antacids for the the gastric discomfort accompanying DKA or alcoholic ketoacidosis may also result in this acid-base disturbance
  • if acidosis is of high anion gap type the presence of a high anion gap may be a clue to a hidden metabolic acidosis
    • In patients with high anion gap acidosis the rise in anion gap should be equal to fall in bicarbonate
  • however a high anion gap is not unequivocal evidence of metabolic acidosis. May be moderately increased and occasionally may be gtr than 25 mmol/L in metabolic alkalosis. Increase in unmeasured anions in metabolic alkalosis is due principally to increased albumin anions. Release of protons by albumin acting as a buffer increases the number of anions per molecule. Plasma albumin concentration may also be increased by associated volume depletion.

Metabolic alkalosis

Causes

Associated with volume (chloride) depletion

- vomiting or gastric drainage
- diuretic therapy
- post-hypercapnic alkalosis

Associated with hyperadrenocorticism

- Cushing's
- Conn's
- Bartter's
- secondary hyperaldosteronism
- steroid therapy

Severe potassium depletion

Excessive alkali intake

- acute
- milk-alkali syndrome

  • usually initiated by increased loss of acid from stomach or kidney
  • excretion of bicarbonate at high plasma concentrations normally so rapid that alkalosis will not be sustained unless bicarbonate reabsorption is enhanced or alkali is continuously generated at a great rate
  • maintenance of alkalosis most often due to stimulation of bicarbonate reabsorption by a volume (chloride) deficit
  • during volume depletion renal conservation of sodium takes preference over other homeostatic mechanisms. In alkalosis a large fraction of plasma sodium is paired with bicarbonate so complete reabsorption of filtered sodium requires reabsorption of bicarbonate as well. Alkalosis is sustained until volume depletion corrected by administration of sodium chloride: diminishes tubular avidity for sodium and provides chloride as an alternative anion for reabsorption with sodium; excess bicarbonate can then be excreted with sodium
  • other major mechanism which can maintain metabolic alkalosis is hypermineralocorticoidism. Elevation of plasma bicarbonate is initiated by increased urinary loss of protons as ammonium and titratable acidity. Stimulation of tubular acid secretion also enhances bicarbonate reabsorption thus sustaining alkalosis. These patients are not volume or chloride depleted
  • respiratory compensation for metabolic alkalosis is limited by hypoxia so PCO2 rarely rises above 7.3-8 kPa
  • up to this level PCO2 increases 0.1 kPa for each mmol/L increase in bicarbonate
  • urinary chloride may be helpful if cause of alkalosis is not evident: low (<10 mmol/L) when alkalosis associated with volume contraction while it is higher (>20 mmol/L) when alkalosis due to hyperadrenocorticism or severe K depletion

Metabolic alkalosis and respiratory acidosis

- in patients with chronic respiratory acidosis due to pulmonary disease metabolic alkalosis is often superimposed by treatment with diuretics, steroids or ventilation. Important to recognize as metabolic alkalosis will reduce acidaemic stimulus to breathe.

Metabolic alkalosis with respiratory alkalosis

- in pregnant patients severe vomiting will superimpose metabolic alkalosis on chronic hypocapnia
- diuretics or vomiting may produce metabolic alkalosis in patients with chronic respiratory alkalosis typical of hepatic cirrhosis
- treatment of cardiac arrest: hyperventilation and bicarbonate therapy plus conversion of lactate accumulated during arrest to bicarbonate. Triple acid-base disorder may occur if circulation not adequately restored: hyperventilation + bicarbonate therapy + lactic acidosis. Anion gap will be high

Respiratory acidosis

- immediate tissue buffering results in only a small rise in plasma bicarbonate (approx. 1 mmol/L for each 1.3 kPa (10 mmHg) rise in PaCO2
- if hypercapnia is sustained renal acid excretion is enhanced and bicarbonate reabsorption is stimulated: over several days plasma bicarbonate rises approximately 3.5 mmol/L for each 1.3 kPa rise in PaCO2
- patients with acute hypercapnia are always acidaemic. Those with chronic hypercapnia are usually acidaemic, however some patients with minimal or moderate hypercapnia may have normal or even slightly raised pH. Significant elevation of pH in patients with chronic hypercapnia is almost always due to co-existent metabolic alkalosis (eg due to diuretics, low-sodium diets or post-hypercapnic alkalosis)

Respiratory alkalosis

- acute reduction in CO2 releases hydrogen ion from tissue buffers: minimize alkalaemia by reducing plasma bicarbonate. Acute alkalosis also enhances glycolysis; increased production of lactic and pyruvic acids lowers serum bicarbonate and raises plasma concentrations of corresponding anions by 1-2 mmol
- chronic hypocapnia: plasma bicarbonate further reduced because decreased PaCO2 inhibits tubular reabsorption and generation of bicarbonate
- compensation: acute - plasma bicarbonate falls about 2 mmol/L for each 1.3 kPa (10 mmHg) fall in PaCO2. Chronic - plasma bicarbonate falls by 4-5 mmol/L for each 1.3 kPa fall in PaCO2

Causes

Hypoxia

  • Acute (eg pneumonia, asthma, pulmonary oedema, hypotension)
  • Chronic (eg pulmonary fibrosis, cyanotic heart disease, high altitude, anaemia)

Respiratory centre stimulation

  • Anxiety
  • Fever
  • Sepsis
  • Salicylate intoxication
  • Cerebral disease (eg tumour, encephalitis)
  • Hepatic cirrhosis
  • Pregnancy
  • After correction of metabolic acidosis
  • Excessive mechanical ventilation

Clinical features

  • tetany probably mainly due to direct enhancement of neuromuscular excitability by alkalosis rather than modest decrease in ionized calcium induced by alkalosis
  • severe respiratory alkalosis may cause confusion or loss of consciousness: may be due to cerebral vasospasm

© Charles Gomersall December 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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