Acid–base disorders - Clinical Tree

Essentials

1
Acid–base homeostasis is one of the most tightly regulated systems within the body. It is maintained by buffering, respiratory and renal mechanisms.
2
Most acid–base disturbances are complex and require a systematic approach to determine underlying processes.
3
High-anion-gap metabolic acidosis and respiratory acidosis are both common in emergency medicine and should direct the clinician to determine and treat the aetiology.
4
Administration of NaHCO ₃ is not routine; however, it is indicated in severe hyperkalaemia, sodium channel blockade and other selected poisonings.
5
Lactate levels greater than 4 mmol/L are associated with raised mortality and should highlight the need for resuscitation and immediate assessment of precipitating pathology.

Introduction

Acid–base disorders are commonly encountered in the emergency department (ED) and their recognition is important for the diagnosis, assessment of severity and monitoring of many disease processes. Although these disorders are usually classified according to the major metabolic abnormality present (acidosis or alkalosis) and its origin (metabolic or respiratory), it is important to realize that acid–base disorders of a mixed type commonly occur, and that the recognition and assessment of these are more complex.

Carbon dioxide (CO ₂ ) produces acid when in solution and altering PaCO ₂ through changes in ventilation can produce or remove acid from the body. The terms respiratory acidosis/alkalosis refer to the pH shifts resulting from alterations in PaCO ₂ from changes in ventilation. Bicarbonate (HCO ₃ ⁻ ) acts as a base in solution with bicarbonate accumulation resulting in a more alkaline state and its wasting or consumption indicating a more acidic state. The terms metabolic acidosis/alkalosis refer to pH shifts characterized by alterations in bicarbonate levels. By convention, the overall pH abnormality as defined by the blood gas assessment is termed alkalaemia (for pH >7.44) or acidaemia (pH <7.34).

Acid–base homeostasis

Acid–base status is one of the most tightly regulated systems in the body. The term compensation is used to describe the processes by which shifts in plasma pH are attenuated. These mechanisms include buffering, respiratory manipulation of CO ₂ and renal handling of bicarbonate. Buffering with plasma proteins, haemoglobin and the carbonic-acid–bicarbonate systems provide the most immediate mechanism. This is followed by respiratory compensation, which occurs within minutes and is achieved by alterations in alveolar ventilation. Renal compensation usually takes hours to days to take effect.

Acidaemia

Systemic acidaemia is defined as the presence of an increased concentration of hydrogen ions ([H ⁺ ]) in the blood. An acidaemia can result from respiratory acidosis, metabolic acidosis or both in combination. The physiological effects of acidaemia are a decrease in the affinity of haemoglobin for oxygen and an increase in serum K ⁺ of approximately 0.4 to 0.6 mmol/L for each decrease in pH of 0.1. Although the presence of acidaemia is often associated with a poor prognosis, the presence of acidaemia per se usually has few clinically significant effects. It is the nature and severity of the underlying illness that principally determines the outcome.

Metabolic acidosis

Metabolic acidosis is defined as an increase in the [H ⁺ ] of the blood as a result of increased acid production or bicarbonate wasting from the gastrointestinal (GI) or renal tract. The cause is often multifactorial and can be further classified into ‘anion-gap’ and ‘non-anion-gap’ (or hyperchloraemic) metabolic acidosis.

High-anion-gap metabolic acidosis ( Table 12.1.1 )

As electro-neutrality must exist in all solutions, the anion gap represents the concentration of anions that are not commonly measured. The most commonly used formula for the calculation of the anion gap is:

AG = [{Na}^{+}] - ([{Cl}^{-}] + [{HCO}_{3}^{-}])

$AG = [{Na}^{+}] - ([{Cl}^{-}] + [{HCO}_{3}^{-}])$

The normal value for the anion gap depends on the type of biochemical analyser used and, while the upper limit of normal has been commonly quoted as 14, the mean range with some modern analysers is only 5 to 12. In the normal resting state, the serum ionic proteins account for most of the anion gap, with a lesser contribution from other ‘unmeasured’ anions, such as phosphate (PO ₄ ⁻ ) and sulphate (SO ₄ ⁻ ). In pathological conditions where there is an increase in the concentration of unmeasured anions, high-anion-gap metabolic acidosis (HAGMA) results. The anions responsible for the increase in the anion gap depends on the cause of the acidosis. Lactic acid is the predominant anion in hypoxia and shock, PO ₄ ⁻ and SO ₄ ⁻ in renal failure, keto-acids in diabetic, alcoholic and starvation keto-acidosis, glycolic, glyoxylic and oxalic acid in ethylene glycol poisoning and formic acid in methanol poisoning.

Of the causes of a HAGMA, lactic acidosis is the most commonly encountered in the ED and is defined as a serum lactate of >2.5 mmol/L ( Box 12.1.1 ). The presence of lactic acidosis is determined by the balance between lactate production and metabolism. In the seriously ill patient, it is common for increased production and decreased metabolism to be present simultaneously.

Box 12.1.1

Causes of hyperlactataemia

Type A: imbalance between oxygen demand and supply	Type B: metabolic derangements
Carbon monoxide poisoning Cyanide poisoning Iron poisoning Isoniazid poisoning Excessive oxygen demand Seizure Hyperpyrexia Shivering Exercise Shock Severe anaemia Hypoxia	Beta ₂ -agonists Cancer Ethanol Hepatic failure Inborn errors of metabolism Ketoacidosis Metformin/Phenformin Sepsis Vitamin deficiency (thiamine, biotin) Paracetamol poisoning Salicylate poisoning

Box 12.1.2

Causes of non-anion-gap metabolic acidosis

GIT Bicarbonate Loss	Renal bicarbonate loss
Diarrhoea Small bowel fistula Pancreatic fistula	Uretoenterostomy Renal tubular acidosis Adrenal insufficiency
Drugs	Excess chloride administration
Carbonic anhydrase inhibitors Acetazolamide Topiramate Acidifying agents Ammonium chloride Cholestyramine

GIT, Gastrointestinal tract.

Box 12.1.3

Causes of low-anion-gap metabolic acidosis

Increased unmeasured cations	Artefactual
Hypercalcaemia Hypermagnesaemia Lithium Multiple myeloma and other gammopathies Dilution	Bromism Iodism Hypoalbuminaemia Hypertriglyceridaemia

Box 12.1.4

Causes of respiratory acidosis

Acute respiratory acidosis	Chronic respiratory acidosis
Airway obstruction Aspiration Bronchospasm Drug-induced CNS depression Hypoventilation of Central Nervous System (CNS) origin e.g. Cerebral tumour Hypoventilation of Peripheral Nervous System (PNS) origin e.g. Guillain-Barré Syndrome (GBS) or Organophosphate (OP) poisoning Pulmonary disease	Pulmonary disease e.g. emphysema, pulmonary fibrosis Neuromuscular disorders e.g. muscular dystrophy Obesity Severe kyphoscoliosis

Box 12.1.5

Causes of metabolic alkalosis

Chloride responsive (Urinary chloride <10 mmol/L)	Chloride unresponsive (Urinary chloride >20 mmol/L
Gastrointestinal losses Vomiting Nasogastric suctioning Bulimia nervosa Pyloric stenosis Tetrahydrocannabinol (THC)-induced cyclical vomiting Diuretics Chloride losing enteropathy Chloride losing nephropathy	Bartter syndrome Liddle syndrome Gitelman syndrome Liquorice excess (glycyrrhizic acid) Conn syndrome (primary hyperaldosteronism) Excess bicarbonate administration Antacids Dialysis Milk-alkali syndrome

Box 12.1.6

Causes of respiratory alkalosis

Central nervous system-mediated hyperventilation	Pulmonary-mediated hyperventilation
Psychogenic Raised intracranial pressure Cerebrovascular accidents	Congestive cardiac failure Mechanical hyperventilation Pulmonary emboli Pneumonia

Hypoxia-mediated hyperventilation	Toxin-induced hyperventilation
Altitude Anaemia V/Q mismatch Sepsis	Salicylates Nicotine Xanthines Caffeine Sympathomimetics

It is important to realize that in many conditions, a variety of factors may produce the acidosis and that multiple anions may be involved in the production of anion-gap acidosis. In a patient with HAGMA, non-anion-gap metabolic acidosis may also co-exist.

Non-anion-gap metabolic acidosis ( Box 12.1.2 )

Non-anion-gap metabolic acidosis results from the loss of HCO ₃ ⁻ from the body, rather than from increased acid production. To maintain electro-neutrality, chloride is usually retained by the renal tubules when HCO ₃ ⁻ is lost and the hallmark of non-anion-gap acidosis is an elevation of the serum chloride. The causes of non-anion-gap metabolic acidosis are further classified according to the site of HCO ₃ ⁻ loss. GI losses can occur with lower GI tract (GIT) fluid losses that are rich in HCO ₃ ⁻ or with cholestyramine ingestion due to binding of HCO ₃ ⁻ in the gut. Renal losses can occur with renal tubular acidosis (RTA), carbonic anhydrase inhibitor therapy or adrenocortical insufficiency. Occasionally, direct chloride excess drives the renal bicarbonate loss (again due to electroneutrality)—which can be observed with large volumes of chloride-rich crystalloid administration (chiefly normal saline).

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