Metabolic alkalosis

• A primary rise in plasma [HCO3 –] may occur in the

following situations:

_ Bicarbonate administration, such as the ingestion of large amounts of

HCO3 to treat indigestion

(milk–alkali syndrome, which is rare) or during intravenous HCO3 infusion

_ Severe K+ depletion with the generation of HCO3 by the kidney

_ Loss of H+: if a H+ is excreted, a HCO3 is gained in the extracellular
space

The most likely loss of H+ is through either the kidneys or the

gastrointestinal tract.
renal losses occur
when the distal tubule [Na+] absorption increases
in the presence of excessive aldosterone, which
stimulates the electrogenic epithelial Na+ channel in
the collecting duct. As this channel reabsorbs Na+,
the tubular lumen becomes more negative, resulting
in H+ and K+ secretion into the lumen. In the case
of the gastrointestinal tract, nasogastric suction or
vomiting causes loss of gastric secretions, which are
rich in hydrochloric acid.
Causes of metabolic alkalosis :
Saline responsive (urine chloride £ 20 mmol/L)
Consider volume-depleted states
Ingestion of exogenous alkalis, e.g. milk–alkali syndrome
(rare) or salts of strong acids, previous diuretic use or
poorly reabsorbable anions, e.g. penicillin
Chloride loss from gastrointestinal tract, e.g. vomiting,
gastric suction, chloride-losing diarrhoea
Chloride loss from skin, e.g. cystic fi brosis
Saline unresponsive (urine chloride > 20 mmol/L)
Certain drugs such as current diuretic therapy or
exogenous mineralocorticoids, e.g. liquorice or
carbenoxolone
Severe hypokalaemia
Severe hypomagnesaemia
Endogenous mineralocorticoid excess, e.g. Cushing’s
syndrome, primary hyperaldosteronism (Conn’s
syndrome), 11-hydroxylase and 17-hydroxylase deficiency
Respiratory alkalosis
The primary abnormality in the bicarbonate
buffer system in respiratory alkalosis is a fall
in PCO2. This is due to abnormally rapid or
deep respiration when the CO2 transport
capacity of the pulmonary alveoli is relatively
Normal.
The compensatory fall in plasma {HCO3}
tends to correct the pH
Some causes of a respiratory alkalosis
-Hyperventilation, e.g. anxiety states, increased
mechanical ventilation
-Exogenous agents that increase respiratory drive,
e.g. salicylates, theophylline, catecholamines,
nikethamide, doxapram, thyroxine and progestogens
-Hypoxaemia due to early and non-severe pulmonary
disease, e.g. asthma, pulmonary embolus,
pneumonia, or high altitude
-Increased cerebral respiratory centre drive, e.g. head
injury, cerebral tumour, meningitis, cerebrovascular
accidents
- Increased non-cerebral causes of respiratory centre
drive, e.g. pregnancy, heat exposure, hepatic failure,
septicaemia
Factors affecting blood gas results
In respiratory acidosis it is often important to know the
partial pressure of oxygen (PO2) as well as the pH, PCO2
and (HCO3).
Normal gaseous exchange across the pulmonary
alveoli involves loss of CO2 and gain of O2. However,
in disease a fall in PO2 and a rise in PCO2 do not always
coexist. The reasons for this are as follows:
1- Carbon dioxide is much more soluble in water than
O2 and its rate of diffusion is about 20 times as high.
For example, in pulmonary oedema, diffusion of O2
across alveolar walls is hindered by oedema fluid and
arterial PO2 falls. The hypoxia and alveolar distension
stimulate respiration and CO2 is excreted.
2-Haemoglobin in arterial blood is normally 95 per cent
saturated with O2, and the small amount of O2 in
simple solution in the plasma is in equilibrium with
oxyhaemoglobin. Increased air entry at atmospheric
PO2 cannot significantly increase O2 carriage in
blood leaving normal alveoli, but can reduce the
PCO2. Breathing pure O2 increases arterial PO2, but
not Hb saturation.
3- In conditions such as lobar pneumonia, pulmonary
collapse and pulmonary fibrosis or infiltration, not
all alveoli are affected equally. At first the gaseous
composition of blood leaving them is normal.
Increasing the rate or depth of respiration may later
lower the PCO2 considerably, but does not alter either
the PO2 or the Hb saturation.
4- Obstruction of small airways means that air cannot
reach those alveoli supplied by them; the composition
of blood leaving them will be near that of venous
blood and there is a ventilation/perfusion mismatch
with a right-to-left shunt.