Discuss the treatment and management of metabolic acidosis and respiratory alkalosis.

(Risk
factors)

Metabolic acidosis is diagnosed when the serum bicarbonate concentration is decreased to a level
less than 15 mEq/l this is because decreased bicarbonate concentration can also be a compensatory
response to respiratory alkalosis. Arterial blood gas analysis is also used to determine metabolic
acidosis by showing low a pH, less than 7.40 and decreased PaCO2. Diagnosis involves evaluating
serum electrolytes and ABGs. Anion gap is calculated to help the d/dx and also to diagnose mixed
disorders. High anion gap acidosis is present if the AG is > than 10-12 mEq/l and a non-AG acidosis is
present if the AG < or equal to 10-12 mEq/l, also AG decreases by 2.5mEq/l for every 1g/dL decrease
of serum albumin.

Elevated AG indicates that osmolar gap should be calculated and this elevated AG can be seen in
ethylene glycol (I believe this is coolant) and methanol poisoning. Other tests such as a screen for
toxins and tests for metabolic disorders e.g. ketoacidosis, lactic acidosis can be performed as these
disorders are known to elevate AG. If AG is not elevated, urinalysis is performed, evaluating pH and
urine AG is calculated and this differentiates between Gi and renal loss of bicarbonate in non- AG
metabolic acidosis. The change in AG helps in detecting a second acid base disorder in patients with
elevated AG. (AG-10)/ (24 -HCO3-). A value of less than 1 indicates presence of a mixed metabolic
acidosis such as non- AG acidosis or high AG acidosis. A value greater than 1.6 indicates the presence
of a mixed acidosis and metabolic alkalosis.

Treatment of metabolic acidosis involves the use of alkali therapy which increases and maintains the
plasma pH to greater than 7.20. If the serum pH is less than 7.20, and the bicarbonate concentration
continues to decrease this can result in a significant decrease in pH especially when the PCO2 is close
to the lower limit of compensation (about 15 mmHg in healthy individuals). As age increases
together with additional complications the limit of compensation is less therefore a small drop in
HCO3- does not correspond to a fall in PCO2 and rapid decompensation can occur. Bicarbonate
correction is also considered in patients with impending respiratory failure as the metabolic acidosis
would increase ventilatory drive to lower the PCO2, however, this may not be sustainable due to
fatigue of the respiratory muscles and the increase in the PCO2 could change the pH dramatically
without a fall in bicarbonate.

In lactic acidosis and diabetic ketoacidosis the organic anion can regenerate the bicarbonate when
the disorder is corrected and there must be caution when trying to correct the acidosis with
bicarbonate therapy unless the pH is less than 7.0-7.1.

The common agent used would be sodium bicarbonate to correct metabolic acidosis. It can
administered intravenously and orally (in some cases) to raise the serum bicarbonate level to
increase the pH to greater than 7.20 and further correction may be needed depending on the
individual situation. We also need to be cautious because for example in high AG acidosis secondary
to accumulation of organic acids, lactate and ketones, they would eventually be metabolized to
HCO3- and therefore when the disorder is treated, overshoot alkalosis may occur.

To minimise hypernatremia and hyperosmolality you could either use three 50 ml ampules of
NaHCO3 to 1 L of 5% dextrose in water or two ampules of 8.4% NaHCO3 to 1 L of 0.25 normal saline.
As aa result of alkali therapy, there can also be volume overload and loop diuretics could used which
inhibit the sodium- potassium- chloride cotransporter in the thick ascending limb of the loop of
Henle and increase urine flow or diuresis.
Oral administration is preferred in chronic metabolic acidosis and this can be in the form of NaHCO3
tablets in 325 or 650mg strengths.

Potassium citrate can also be used when the acidosis is accompanied with hypokalaemia but should
be used cautiously if there is renal impairment and must not be used if there is hyperkalaemia.
Citrates salts are available in a variety of formulations such as mixtures of citric acid with sodium
citrate or potassium citrate. Risk factors include diarrhea, ketogenic diet, underlying renal or lung
disease, and surgery

Type 1 renal tubular acidosis
Type 2 renal tubular acidosis
Type 4 renal tubular acidosis
Chronic kidney disease
Administration of alkali, patients are given the
amount to buffer the daily acid load form the
diet, approx.. 1-3 mEq/kg/day administered in
any form, potassium citrate is preferred,
hypokalaemia is corrected but in some cases,
K+ supplements may be needed
Correction is difficult as large proportion of the
HCO3- administered is excreted in the urine,
therefore large amounts are needed together
with potassium. Correction is essential in
children for normal growth, however, in adults
such aggressive correction may not be
required. Thiazide diuretics can also be used to
induce diuresis
Hyperkalaemia is primarily the cause of this
disorder and therefore treatment involves
lowering serum K+ levels, either by placing the
patient on a low K+ diet or withdrawal of drugs
that can cause hyperkalaemia such as ACE
inhibitors, or NSAIDS. If the patient is not
hypovolemic, loop diuretics can be used to
reduce serum K+ levels. In more resistant cases,
fludrocortisone which is a synthetic
mineralocorticoid, can be used to increase K+
secretion but this may increase Na retention.
Alkali therapy is not usually required.
Treatment prevents bone loss that can progress
into osteopenia or osteoporosis, in children it
can prevent growth retardation. Also,
treatment slows the progression of
hyperparathyroidism which would help reduce
high protein catabolism associated with uremic
acidosis which can result in reduction of muscle
mass and malnutrition.
Alkali treatment is administered to decrease
muscle wasting and improve bone health, in
patients with 3b and 4 CKD, it improves
vascular endothelial function.
Treatment can also include dietary
modifications such as reducing the intake of
acid producing foods such as animal proteins,
emphasizing the use of base producing foods
 such as fruits and vegetables
Ketoacidosis Due to starvation and alcohol use. Treated
using intravenous glucose which stimulates
insulin secretion and would therefore stop
lipolysis and ketosis.
In diabetic ketoacidosis, insulin is administered
intravenously, to facilitate cellular uptake of
glucose , reduce gluconeogenesis and halt
lipolysis and production of ketone bodies.
Normal saline is also administered to reduce
extracellular volume, K and phosphate
replacement may be necessary. The acidosis is
corrected partly by metabolism of ketones to
HCO3- , increased H+ secretion by collecting
ducts and H+ excretion as NH4+
Lactic acidosis Correction of underlying disorder. Patients with
tissue hypoxia requires restoration of tissue
perfusion.
Salicylate poisoning Initiate alkaline diuresis by IV NaHCO3 or
acetazolamide therapy. The goal of therapy is
to maintain a urine pH greater than 7.5 until
salicylate level falls below 30- 50 mg/dL.
Multiple doses of activated charcoal is also
used
Methanol or ethylene glycol poisoning Fomepizole, a potent inhibitor of alcohol
dehydrogenase is the preferred therapy.
HCO3- therapy can be administered to correct
severe acidosis but large amounts may be
required resulting in fluid overload which can
compromise therapy.
Folate can be used in methanol overdose.
Thiamine and pyridoxine can be used in
ethylene glycol overdose.
Haemodialysis is also considered if there is
renal failure, visual symptoms, high toxin level
or suspected large overdose.

Treatment of respiratory alkalosis primarily involves correcting the underlying disorder. Respiratory
itself is rarely life threatening hence emergency treatment is not usually required unless the pH
exceed 7.5. as it usually occurs in response to some stimulus, treatment is not successful unless the
stimulus is controlled. If the PC02 is corrected rapidly, metabolic acidosis may result due to a renal
compensatory drop in serum bicarbonate.

In mechanically ventilated patients, respiratory rate may need to be decreased.

In hyperventilation syndrome, reassurance of the patient, rebreathing into a paper bag during acute
episodes and psychological treatment is effective. Also sedatives or antidepressants can be used but
must be used to patients not responding to conservative treatment. Beta adrenergic blockers may
also help hyperventilation syndrome in some patients.