DISORDERS OF ACID-BASE BALANCE

The pH (the negative logarithm of [H+]) is maintained at 7.4 (normal range 7.35-7.45). The metabolism of food and endogenous body tissues produces about 70-100 mmol of H+ each day, which is excreted by the kidneys. Bicarbonate (HCO3-) is the main plasma and extracellular fluid buffer. It mops up free H+ ions and prevents increases in the H+ concentration (Fig. 8.4). Bicarbonate is filtered at the glomerulus but is then reabsorbed in the proxi-mal and distal renal tubule. The lungs also constantly regulate acid-base balance through the excretion of CO2. Between production and excretion of H+ ions there is an extremely effective buffering system maintaining a con-stant H+ ion concentration inside and outside the cell. Buffers include hae-moglobin proteins, bicarbonate and phosphate.

Fig. 8.4 The carbonic anhydrase reaction.

Acid-base disturbances may be caused by:

■ Abnormal carbon dioxide removal in the lungs ('respiratory' acidosis and alkalosis)

■ Abnormalities in the regulation of bicarbonate and other buffers in the blood (‘metabolic' acidosis and alkalosis).

In general, the body compensates to some extent for changes in pH by regu-lating renal bicarbonate excretion and altering the respiratory rate. For instance, metabolic acidosis causes hyperventilation (via medullary chemo-receptors), leading to increased removal of CO2 in the lungs and partial compensation for the acidosis. Conversely, respiratory acidosis is accompa-nied by renal bicarbonate retention, which could be mistaken for primary metabolic alkalosis.

Measurement of pH, Paco2 and [HCO3-] will reveal which type of distur-bance is present (Table 8.8). These measurements are made on an arterial blood sample using an automated blood gas analyser. Clinical history and examination usually point to the correct diagnosis. In complicated patients, the Flenley acid-base nomogram can be used to identify the acid-base disorder that is present when arterial hydrogen ion concentration and Paco2 are known (Fig. 8.5).

Respiratory acidosis

This is usually associated with ventilatory failure, with retention of carbon dioxide (p. 584). Treatment is of the underlying cause.

Respiratory alkalosis

Hyperventilation results in increased removal of carbon dioxide, resulting in a fall in PaCO2 and [H+].

Table 8.8 Changes in arterial blood gases

pH

Paco2

HCO3-

Acidosis

Metabolic

Normal or reduced

Normal or reduced

Reduced ++

Respiratory

Normal or reduced

Increased ++

Normal or increased

Alkalosis

Metabolic

Normal or increased

Increased

Increased ++

Respiratory

Normal or increased

Reduced ++

Reduced

The pH may be at the limits of the normal range if the acidosis or alkalosis is compensated, e.g. respiratory compensation (hyperventilation) of a metabolic acidosis.

The clue to the abnormality from the blood gases will be the abnormal PaCO2 and HCO3-

The Flenley acid–base nomogram

Fig. 8.5 The Flenley acid-base nomogram.

Metabolic acidosis

This is the result of the accumulation of any acid other than carbonic acid. The most common cause is lactic acidosis following shock or cardiac arrest.

Clinical features

These include hyperventilation, hypotension caused by arteriolar vaso-dilatation and the negative inotropic effect of acidosis, and cerebral dys-function associated with confusion and fits.

Differential diagnosis (the anion gap)

The first step is to identify whether the acidosis is the result of retention of HCl or of another acid. This is achieved by measurement of the anion gap. The main electrolytes measured in plasma are sodium, potassium, chloride and bicarbonate. The sum of the cations, sodium and potassium normally exceeds that of chloride and bicarbonate by 6-12 mmol/L. This anion gap is usually made up of negatively charged proteins, phosphate and organic acids. If the anion gap is normal in the presence of acidosis, it can be concluded

Table 8.9 Causes of metabolic acidosis with a normal anion gap
Increased gastrointestinal HCO3- loss
Diarrhoea
Ileostomy
Ureterosigmoidostomy
Increased HCO3
− renal loss
Acetazolamide ingestion
Proximal (type 2) renal tubular acidosis
Hyperparathyroidism
Tubular damage, e.g. drugs, heavy metals
Decreased renal H+ excretion
Distal (type 1) renal tubular acidosis
Type 4 renal tubular acidosis
Increased HCl production
Ammonium chloride ingestion
Increased catabolism of lysine, arginine

that HCl is being retained or NaHCO3 is being lost. The causes of a normal anion gap acidosis are given in Table 8.9.

If the anion gap is increased (i.e. >12 mmol/L), the acidosis is the result of an exogenous acid, e.g. salicylates or one of the acids normally present in small unmeasured quantities, such as lactate. Causes of a high anion gap acidosis are given in Table 8.10.

Lactic acidosis

Increased production of lactic acid occurs when cellular respiration is abnor-mal, resulting from either lack of oxygen (type A) or a metabolic abnormality (type B). The most common form in clinical practice is type A lactic acidosis, occurring in septicaemic or cardiogenic shock.

Diabetic ketoacidosis

This is a high anion gap acidosis caused by the accumulation of acetoacetic and hydroxybutyric acids.

Renal tubular acidosis

Renal tubular acidosis may occur in the absence of chronic kidney disease and is a normal anion gap acidosis. There is failure of the kidney to acidify the urine adequately. This group of disorders is uncommon and only rarely a cause of significant clinical disease. There are four types of which type 4 (also known as hyporeninaemic hypoaldosteronism) is the most common. Typical features are acidosis and hyperkalaemia occurring in the setting of mild chronic kidney disease, usually caused by tubulointerstitial disease or

Table 8.10 Causes of metabolic acidosis with a high anion gap

Renal failure (sulphate, phosphate)
Ketoacidosis
Diabetes mellitus
Starvation
Alcohol poisoning
Lactic acidosis
Type A
Shock
Severe hypoxia
Methanol ingestion
Ethylene glycol ingestion
Strenuous exercise
Type B
Acute liver failure
Poisoning: ethanol, paracetamol
Metformin accumulation
Leukaemia, lymphoma
Drug poisoning
Salicylates

diabetes. Plasma aldosterone and renin levels are low and do not respond to stimulation. Treatment is with fludrocortisone, diuretics, sodium bicarbonate and ion exchange resins for the reduction of serum potassium.

Uraemic acidosis

Reduction of the capacity to secrete H+ and NH4+, in addition to bicarbonate wasting, contributes to the acidosis of chronic kidney disease. Acidosis occurs particularly when there is tubular damage, such as reflux and chronic obstructive nephropathy. It is associated with hypercalciuria and renal osteodystrophy because H+ ions are buffered by bone in exchange for calcium. Treatment is with calcium or sodium bicarbonate, although acidosis in end-stage renal failure is only usually fully corrected by adequate dialysis.

Metabolic alkalosis

This is much less common than acidosis and is often associated with potas-sium or volume depletion. The main causes are persistent vomiting, diuretic therapy or hyper-aldosteronism. Vomiting causes alkalosis both by causing volume depletion and through loss of gastric acid.

Clinical features

Cerebral dysfunction is an early feature of alkalosis. Respiration may be depressed.

Management

This includes fluid replacement, if necessary, with replacement of sodium, potassium and chloride. The bicarbonate excess will correct itself.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology

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