In health, blood hydrogen ion concentration
lies within the range pH 7.3 6—7.44. The terms acidosis and alkalosis in
clinical practice indicate a change or a tendency to a change in the pH of the
blood in a particular direction. In acidosis, there is an accumulation of acid
or a loss of a base causing a fall or a tendency to a fall in the pH. The
converse occurs in alkalosis. The pH of the blood is regulated and controlled by
various buffering systems essentially consisting of weak acids and bases, of
which the most important is the bicarbonate:carbonic acid ratio HCO3:H2C03.
It is also regulated by the removal of carbon dioxide by the lungs and by the
excretion of both acids and bases by the kidneys.
The
ratio of bicarbonate to carbonic acid is normally 20:1. Alteration in this ratio
alters the pH regardless of the absolute values of the bicarbonate and carbonic
acid. A decrease in the ratio leads to increased acidity and vice versa.
The
bicarbonate level can be altered by metabolic factors, while the carbonic acid
level is subject to alteration by respiratory factors. Alteration of one is
followed automatically by a compensatory alteration in the other, so that the
ratio (HCO3:H2C03) and therefore the pH of the
blood remains constant.
Measurement of
acid—base disturbances
These measurements are normally made on
arterial or materialized capillary blood. PCO2 is a measurement of
the tension or partial pressure of carbon dioxide in the blood. The normal
arterial PCO2 is 4.1—5.6 kPa
(31—42 mmHg). P02 is a measurement of the tension or partial
pressure of oxygen in the blood. The normal arterial P02 is 10.5—14.5
kPa (80—110 mmHg).
Standard bicarbonate
is the
concentration of the serum bicarbonate after fully
oxygenated blood has been equilibrated with carbon dioxide at 40
mmHg (5.3 kPa) at 380C. This eliminates respiratory causes and
respiratory compensation for altered bicarbonate levels. Normal levels are
22—25 mmol/litre.
Base excess or deficit expresses,
in mmol, the total buffer anions present in the blood in excess of deficit of
normal. (Normal base excess or deficit +
2.5.) Base excess or deficit multiplied by 0.3 times the body weight in
kg gives the total extracellular excess or deficit of base in mmol. Metabolic
causes of acid—base disturbances are indicated by changes in the standard
bicarbonate level and base excess or deficit. Respiratory causes of acid—base
disturbances are indicated by changes in the PCO2 and P02.
Alkalosis
Metabolic alkalosis, a condition of base excess or a deficit of any acid
other than H2C03, can be caused by:
•
excessive ingestion of absorbable alkali. This is not uncommon in
patients who take proprietary indigestion remedies without medical supervision;
•
loss of acid from the stomach by repeated vomiting or aspiration;
•
cortisone excess, usually the result of over-administration of adrenal
corticoids, but occasionally due to Cushing’s syndrome (see Chapter 44).
Compensation
is effected by: (a) retention of carbon dioxide by the lungs; and (b) excretion
of bicarbonate base by the kidneys (alkaline urine).
Clinical features.
Alkalosis
due to loss of acid from the stomach is the most common and most important. In
its most typical form, it is seen in patients with pyloric stenosis in whom the
loss of acid by repeated vomiting is often accentuated by the taking of
medicines containing sodium bicarbonate. The most striking feature of severe
alkalosis is Cheyne—Stokes respiration with periods of apnoea lasting from 5
to 30 seconds. Tetany sometimes occurs. Latent tetany is more common, and
can be unveiled by Trousseau s sign (see Chapter 44). Regarding other signs, the
dual phenomenon of severe alkalosis and hypokalaemia is so interwoven that
their clinical separation is well-nigh impossible. Subclinical degrees of
alkalosis are recognisable only by a raised standard bicarbonate concentration
and a positive base excess. Severe alkalosis may result in renal epithelial
damage and consequent renal insufficiency.
Treatment.
Metabolic
alkalosis without hypokalaemia seldom requires direct treatment. The cause of
the alkalosis should be removed where possible and a high urinary output
encouraged.
Hypokalaemic alkalosis
Hypokalaemic alkalosis is seen in patients who
have lost potassium and acid owing to repeated vomiting from pyloric stenosis.
The low serum potassium causes potassium to leave the cell and be replaced by
Na+ and H+ ions. The shift of H+ ion into the cell causes intracellular acidosis
and increases the cellular acidosis of the kidney cells.
Treatment.
When hypokalaemia is sufficient to cause a metabolic alkalosis, the losses can
be massive (> 1000 mmol). Replacement is a serious undertaking (see above).
It can be achieved gradually and relatively safely by supplementing intravenous
fluids with 40 mmol/litre of KCI if the urine output is adequate. More rapid
replacement (up to 60 mmol/hour) will require intensive monitoring and
supervision
with continuous ECG monitoring in a high dependency or intensive care
environment.
Respiratory alkalosis
Respiratory alkalosis, a condition where the
arterial PCO2 is below the normal range of 31—42 mmHg (4.1—5.6
kPa), is caused most commonly in surgical practice by excessive pulmonary
ventilation carried out upon an anaesthetised patient. Other causes are
hyperventilation occasioned by high altitudes, hyperpyrexia, a lesion of the
hypothalamus and hysteria. Compensation, which depends on increased renal
excretion of bicarbonate, usually is inadequate. During anaesthesia alkalosis is
accompanied by pallor and a fall in blood pressure. In severe cases respiratory
arrest follows.
Treatment.
Respiratory
suppression due to alkalosis is rectified by insufflation of carbon dioxide.
Acidosis
Metabolic acidosis, a condition where there is
a deficit of base or an excess of any acid other than H2C03,
occurs as a result of:
• increase in fixed acids due to the formation of ketone bodies as in
diabetes or starvation, the retention of metabolites in renal insufficiency, and
the rapid increase of lactic and pyruvic acids by anaerobic tissue metabolism,
following cardiac arrest, or the release of the clamped aorta in the surgery of
abdominal aneurysm. Acute acidosis with pH levels of 7.1 is frequently
encountered in such cases;
• loss of bases such as occurs in sustained diarrhoea, ulcerative
colitis, gastrocolic fistula, a high intestinal fistula or prolonged intestinal
aspiration.
In
severe acidosis, the leading sign is rapid, deep, noisy breathing. The
hyperpnoea is due to over stimulation of the respiratory centre by the reduction
in pH of the blood, and the physiological purpose of overbreathing is to
eliminate as much as possible of the acid substance H2C03.
Except in renal acidosis, the urine is strongly acidic. The standard bicarbonate
level is lowered and there is a base deficit.
Treatment.
The
commonest cause of an acute peroperative metabolic acidosis is tissue hypoxia
and the correct treatment is restoration of adequate tissue perfusion. Treatment
with bicarbonate solutions will correct the measured metabolic acidosis but not
treat the problem. Indeed, as bicarbonate is rapidly converted into carbon
dioxide intracellular acidosis may, in fact, get worse. The administration of
bicarbonate solutions should be reserved solely for situations where bases have
been lost or where the degree of acidosis is so severe that myocardial function
is compromised (this is rare).
The
acute acidosis seen in prolonged cardiac arrest may require the infusion of 50
mmol of 8.4 per cent sodium bicarbonate solution.
Acidosis due to transplantation of the ureters into the colon
Respiratory acidosis, a condition where the
PCO2 is above the normal range, is caused by impaired alveolar
ventilation.
In
practice this problem most commonly occurs when there is inadequate ventilation
of the anaesthetised patient, or when the effects of muscle relaxants have not
worn off or been fully reversed at the end of the anaesthetic. There is also a
risk of respiratory acidosis when the patient undergoing surgery already has
pre-existing pulmonary disease (e.g. chronic bronchitis or emphysema), and this
is accentuated by thoracic and upper abdominal incisions.
The anion gap
This is a calculated estimation of the
undetermined or unmeasured anions in the blood. It is sometimes used to
establish
the cause of a metabolic acidosis. Anion gap = (Na + K)