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Disturbances of acid–base homeostasis 

Disturbances of acid–base homeostasis

Chapter:
Disturbances of acid–base homeostasis
Author(s):

R. D. Cohen

and H. F. Woods

DOI:
10.1093/med/9780199204854.003.1211_update_001

November 28, 2013: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

Update:

New or enhanced discussion of lactic acidosis due to cyanide poisoning, pyroglutamic acidaemia, acidosis in the Wolcott–Rallison syndrome, and lactic acidosis in malignancy.

Updated on 30 Nov 2011. The previous version of this content can be found here.
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date: 25 March 2017

Acid–base physiology and terminology

Despite a daily load of protons, derived mainly from metabolism, the hydrogen ion concentration of arterial blood in health is tightly maintained within a slightly alkaline range (pH 7.36–7.42); concentrations of intracellular hydrogen ions are also controlled. Failure adequately to excrete or neutralize protons causes acidic conditions to prevail (decreased pH): undue intake of base, uncompensated loss of protons—or the substrates from which they are derived—induces an alkaline milieu (raised pH).

The term acidosis refers to the pathological reduction of pH, also to the circumstance when pH would have been decreased were it not for the occurrence of compensatory mechanisms; an equivalent but reciprocal definition applies to alkalosis.

In health, the principal source of protons is CO2, which originates from aerobic metabolism, is volatile and thus eliminated readily by the lungs. Lesser contributions come from urea synthesis and the generation of lactate and other organic anions such as 3-hydroxybutyrate and acetoacetate, which are eliminated by metabolism in the liver, kidneys and other tissues. Less than 1% of the proton burden is derived from the breakdown of sulphur- and phosphorus-containing molecules; these are ultimately converted to non-volatile sulphuric and phosphoric acids, which are excreted exclusively by the kidneys.

The body has limited capacity to offset rapid changes in pH by using extracellular and intracellular buffers, which are chiefly proteins (e.g. haemoglobin) or bicarbonate and phosphate ions. Acid–base buffering allows decompensation to be avoided transiently, but the proton burden must in the end be eliminated.

When the primary acid–base disorder is related to abnormal CO2 elimination, it is termed ‘respiratory’. All other primary disturbances of acid production or elimination are ‘metabolic’. Primary processes are to be distinguished from those that are compensatory, which are termed ‘secondary’, e.g. secondary respiratory alkalosis as a compensatory mechanism for primary metabolic acidosis.

Clinical aspects of acid–base disturbances

Disturbances of acid–base balance have major effects on the body, including respiration, consciousness, cardiac function (acidosis decreases cardiac contractility and alkalosis has a small opposite effect, with both conditions predisposing to cardiac arrhythmia), renal function, and drug metabolism (Moviat, 2008). Potassium homeostasis is critically affected, with hypokalaemia a usual association of metabolic alkalosis and hyperkalaemia of metabolic acidosis.

Primary acid–base syndromes—these include: (1) respiratory acidosis due to respiratory failure; (2) metabolic acidosis due to diabetic ketoacidosis, lactic acidosis from multiple causes, renal acidosis, and poisoning by agents such as salicylate and methanol; (3) respiratory alkalosis due to hyperventilation; and (4) metabolic alkalosis due to the use of potassium-losing diuretics and persistent severe vomiting.

Arterial blood gas analysis—clinical evaluation cannot determine arterial pH, PaCO2, and bicarbonate concentration. Sampling of arterial blood is required. Blood gas analysers measure pH and Pco2 directly, and calculate plasma bicarbonate. They also generally provide at least two other derived acid–base variables that are attempts to provide a measurement independent of respiratory disturbance and thus indicative of any underlying pure metabolic disturbance: (1) standard bicarbonate, which represents what the plasma bicarbonate would be if the blood had the normal PaCO2 of 5.33 kPa (40 mmHg) rather than its actual value; and (2) base excess or deficit, which is the amount of alkali in mmol needed to restore the pH of 1 litre of the patient’s blood in vitro to normal (pH 7.4) at a Pco2 of 5.33 kPa. An acid–base diagram is recommended for interpreting the results. Plasma urea, creatinine, sodium, potassium, and chloride, and—when appropriate—lactate, ketoacid, and salicylate concentrations are useful.

Anion gap—the sum of the concentrations of plasma cations (Na+ and K-) normally exceeds that of the anions (Cl and HCO3). This so-called anion gap (range 10–18 mmol/litre) is usually attributable to the net negative charge on plasma proteins, phosphate, sulphate, and organic acids. Metabolic acidoses may have a high or normal anion gap. Those with a high anion gap are due to the ingestion or endogenous generation of acids, usually organic, whose anions are not routinely measured in plasma. Calculation of the anion gap is therefore valuable for diagnosis of metabolic acidosis, but the regre ttable practice of omitting chloride estimations frequently prevents its application.

Management—the mainstay of treatment of acid–base disorders is to eliminate the cause, with restoration of acid–base balance occurring in due course as physiological control mechanisms are able to compensate. It may occasionally be necessary to restore or partly restore normal acid–base status directly, but some interventions of this kind, e.g. infusion of bicarbonate solutions in metabolic acidosis, remain controversial.

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