REGULATION OF BODY FLUID HOMEOSTASIS

Maintenance of the effective circulating volume is essential for adequate tissue perfusion and is mainly related to the regulation of sodium balance. In contrast, maintenance of osmolality prevents changes in cell volume and is largely related to the regulation of water balance.

Regulation of extracellular volume

The regulation of extracellular volume is determined by a tight control of the balance of sodium, which is excreted by normal kidneys. Although only a small proportion of total extracellular fluid resides in the arterial circulation it is the fullness of the arterial vascular compartment - or the so-called effective arterial blood volume (EABV) - that is the primary determinant of renal sodium and water excretion. The fullness of the arterial compartment depends on a normal ratio between cardiac output and peripheral arterial resistance. Thus, diminished EABV is initiated by a fall in cardiac output or a fall in peripheral arterial resistance (an increase in the holding capacity of the arterial vascular tree). When the EABV is expanded, this in turn leads to an increase in urinary sodium excretion and vice versa.

Two types of volume receptors sense changes in the EABV:

■ Extrarenal: in the large vessels near the heart

■ Intrarenal: in the afferent renal arteriole, which Controls the renin-angiotensin system via the juxtaglomerular apparatus.

A decreased effective circulating volume leads to activation of these volume receptors, which leads to an increase in sodium (and hence water) reabsorp-tion by the kidney and expansion of the extracellular volume via stimulation of the sympathetic nervous system and activation of the renin-angiotensin system (p. 655). In contrast, atrial natriuretic peptide (ANP), produced by the atria of the heart in response to an increase in blood volume, increases sodium excretion.

Abnormalities of extracellular volume

Increased extracellular volume

Extracellular volume expansion is the result of increased sodium (and hence water) reabsorption or impaired excretion by the kidney.

Clinical features

These depend on the distribution of excess fluid within the extracellular space (i.e. between the interstitial space and intravascular compartment), which in turn depends on venous tone (which determines hydrostatic pressure), capil-lary permeability, oncotic pressure (mainly dependent on serum albumin) and lymphatic drainage. For instance, with hypoalbuminaemia there is a reduction in plasma oncotic pressure and predominantly interstitial volume overload. Cardiac failure leads to expansion of both compartments:

■ Interstitial volume overload- ankle oedema, pulmonary oedema, pleural effusion and ascites.

■ Intravascular volume overload - raised jugular venous pressure, cardio-megaly and a raised arterial pressure in some cases.

This must be differentiated from local causes of oedema (e.g. ankle oedema as a result of venous damage following thrombosis), which do not reflect a disturbance in the control of extracellular volume.

Aetiology

Most causes of extracellular volume expansion are associated with renal sodium chloride retention.

■ Cardiac failure due to a reduction in cardiac output and impaired per-fusion (therefore effective hypovolaemia) of the volume receptors. The increased sympathetic activity generated by stimulation of the volume receptors also leads to release of antidiuretic hormone (ADH) even though plasma osmolality (see later) is unchanged.

■ Cirrhosis. This is through a complex mechanism, but there is vaso-dilatation and hence underperfusion of the volume receptors. Hypo-albuminaemia may also contribute.

■ Nephrotic syndrome. Sodium retention is primarily due to increased sodium reabsorption in the renal collecting tubules directly induced by the renal disease. In addition, in some patients the low plasma oncotic pressure induced by hypoalbuminaemia leads to plasma volume depletion and arterial underfiNing as in cardiac failure and cirrhosis.

■ Sodium retention. This may be as a result of renal impairment, where there is a reduction in renal capacity to excrete sodium, or due to drugs such as mineralocorticoids (aldosterone-like actions), thiazolidinediones (by upregulation of epithelial sodium transporter channel) and non-steroidal anti-inflammatory drugs (NSAIDs). The latter inhibit synthe-sis of vasodilatory prostaglandins in the kidney with an increase in renal vascular resistance and increase in water and sodium reabsorption.

Management

The underlying cause must be treated. The cornerstone of treatment, the diuretics, increase sodium and water excretion in the kidney. There are a number of different classes of diuretic, of which the most potent are the loop diuretics, e.g. furosemide (Table 8.4 and p. 349).

Decreased extracellular volume

This may be the result of loss of sodium and water, plasma or blood.

Aetiology

Volume depletion occurs in haemorrhage, plasma loss in extensive burns, or loss of salt and water from the kidneys, gastrointestinal tract or skin (Table 8.5). Signs of volume depletion occur despite a normal or increased body content of sodium and water in sepsis (due to vasodilatation and increased capillary permeability) and diuretic treatment of oedematous states where mobilization of oedema lags behind a rapid reduction in plasma volume due to diuresis.

Clinical features

Symptoms include thirst, nausea and postural dizziness. Interstitial fluid loss leads to loss of skin elasticity ('turgor'). Loss of circulating volume causes

Table 8.4 The main classes of diuretics in clinical use

Class

Example

Mechanism of action

Relative

potency

Loop diuretics

Furosemide

Bumetanide

Reduce Na+ and Cl- reabsorption in ascending limb of loop of Henle

Thiazides

Bendroflumethiazide

Hydrochlorothiazide

Reduce sodium reabsorption in distal convoluted tubule

++

Aldosterone

antagonists

Spironolactone

Eplerenone

Aldosterone antagonist

+

Potassium-sparing

Amiloride

Prevent potassium exchange for sodium in distal tubule

+

Table 8.5 Causes of extracellular volume depletion

Haemorrhage
External
Concealed e.g. leaking aortic aneurysm
Burns
Gastrointestinal losses
Vomiting
Diarrhoea
Ileostomy losses
Ileus
Renal losses
Diuretic use
Impaired tubular sodium conservation
Reflux nephropathy
Papillary necrosis
Analgesic nephropathy
Diabetes mellitus
Sickle cell disease

Investigations

The diagnosis is usually made clinically. A Central venous line allows the measurement of central venous pressure, which helps in assessing the response to treatment. Plasma urea may be raised because of increased urea reabsorption and, later, prerenal failure (when the creatinine rises as well). This is, however, very non-specific. Urinary sodium is low (<20 mmol/L) if the kidneys are working normally. The urinary sodium can be misleading, however, if the cause of the volume depletion involves the kidneys, e.g. with diuretics or intrinsic renal disease.

Management

The aim of treatment is to replace what has been lost.

■ Haemorrhage involves the loss of whole blood. Immediate treatment is with crystalloid or colloid until packed red cells are available.

■ Loss of plasma, as in burns or severe peritonitis, should be treated with human plasma or a colloid (p. 326).

■ Loss of sodium and water, as in vomiting, diarrhoea or excessive renal losses, is treated with replacement of water and electrolytes. In chronic conditions associated with mild/moderate sodium depletion, e.g. salt-losing bowel or renal disease, oral supplements of sodium chloride or sodium bicarbonate (depending on acid-base balance) may be suffi-cient. Glucose-electrolyte solutions are often used to restore fluid balance in patients with diarrhoeal diseases. This is based on the fact that the presence of glucose stimulates intestinal absorption of salt and water (p. 38).

■ In the acute situation if there have been large losses of sodium and water, patients are usually treated with intravenous sodium chloride 0.9% (Tables 8.3), and replacement is assessed clinically and by measurement of serum electrolytes. Rapid infusion (1000 mL/h) of sodium chloride 0.9% or colloid is given if the patient is hypotensive.

■ Loss of water alone, e.g. diabetes insipidus, only causes extracellular volume depletion in severe cases because the loss is spread evenly over all the compartments of body water. The correct treatment is to give water. If intravenous treatment is required, water is given as glucose 5% (pure water is not given because it would cause osmotic lysis of blood cells).

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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