PHYSIOLOGY

The organization and

composition of body fluids

Learning objectives
After reading this article you should be able to:
C
understand how total body water is divided into compartments
and describe how they can be measured experimentally
C
compare the ionic composition of the intracellular and extracellular compartments
C
quantify the typical daily input and output of body fluids of a
70-kg man
C
understand how different types of administered fluids
distribute across these compartments
C
describe the detector and effector mechanisms contributing to
endogenous fluid volume homeostasis
C
understand the regulation of sodium in the body and the
relationship with volume and potassium regulation

Benjamin R Waterhouse
Andrew D Farmery

Abstract
The water contained in the body is divided amongst compartments of
differing sizes and compositions. The dynamic balance across these compartments is an essential component of normal physiology. Here, the
calculation of these volumes by measuring the dilution of markers able
to permeate specific compartments is considered. Furthermore, the potential disadvantages to the approach are discussed. The differences in
ionic concentration between intracellular and extracellular fluid are quantified and the effects of greater relative protein concentration within cells
are also considered. To illustrate daily fluid balance in a healthy individual, a typical intake and output over 24 hours is quantified before consideration of iatrogenic contributions to this equilibrium. The way in which
clinically administered fluids of varying compositions affect the fluid compartments is subsequently discussed. The endogenous processes contributing to volume homeostasis are then deliberated including the detection
of fluid imbalance through intracellular and extracellular systems as well
as the hypothalamic and renal effector mechanisms. Finally, the regulation
of sodium is discussed with examination of the mechanisms controlling
natriuresis and the reciprocity with potassium balance.

represents the plasmaewater volume of 3.5 litres, which with

cellular content forms approximately 5 litres of blood.
This approximate guide to fluid compartments does not hold
true for the whole population, as fairly obvious differences in
body composition are observed. As the proportion of body mass
comprising adipose tissue increases, a comparatively anhydrous
tissue, the contribution of water to body weight will decrease.
Typically females have a greater percentage body fat and so a
lower percentage body weight will be water derived. Similarly,
an increase in age is associated with a greater proportion of body
fat, replacing previously water rich tissues.
The measurement of these values can be achieved using
marker dilution techniques. By introducing a water-soluble dye
into the body that is restricted in its distribution throughout the
compartments the volume of distribution can be calculated from
which the compartment volume can be inferred. In order to estimate TBW, deuterated or tritiated water can be used, as these
will distribute precisely as normal water does. Sodium bromide
or inulin can be used to measure the ECF as they are unable to
cross the cell membranes. The ICF volume can then be calculated
from the difference between TBW and ECF. Finally, radiolabelled albumin or red blood cells can be given intravenously
to quantify plasma volume.
Once a marker has been allowed to equilibrate, the volume of
distribution (V) can be calculated from the total amount injected
(M ), the amount excreted during the time taken to equilibrate
(E ) and the measured concentration. Using Equation 1, this gives
the volume of the compartment being considered:

Keywords Extracellular fluid; fluid balance; fluid compartments; intracellular fluid; ion composition; sodium homeostasis; volume homeostasis; volume of distribution
Royal College of Anaesthetists CPD Matrix: 1A01

Fluid compartments
Fluid volumes
The distribution of body mass for a typical 70-kg man can be
seen in Figure 1. Although approximate, these values can be
useful when considering fluid balance. The majority of the total
body water (TBW) exists within cells in the intracellular fluid
(ICF). While only a third is external to cell membranes in the socalled extracellular fluid (ECF). About 75% of the ECF is outside
the vascular system, primarily in the form of interstitial fluid. It
also includes a small volume that can be considered transcellular, for example cerebrospinal fluid and intra-ocular fluids.
These are defined separately owing to their secretory origins and
enclosure within epithelium-lined cavities. However, as their
water content is not freely available for fluid exchange these will
not be considered in detail. The remaining quarter of ECF

Eq 1

Equation 1. Calculating volume of distribution for an administered marker.

Benjamin R Waterhouse BA BM BCh Academic Foundation Doctor,

North Bristol NHS Trust, UK. Conflicts of interest: none declared.

Elimination of the marker will include metabolism, either

hepatic or cellular, and renal excretion. Correcting for this
metabolized fraction cannot be achieved accurately. The measurement of renal excretion is also cumbersome, requiring the
emptying of the bladder before administration and after

Andrew D Farmery BSc MA MD FRCA Fellow and Tutor in Medicine and

Physiology, Wadham College, Oxford, UK. Conflicts of interest:
none declared.

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Breakdown of total body mass into anhydrous and fluid compartments

70-kg man

60%
[42 litres]
water

2/3
[28 litres]
Intracellular fluid (ICF)

40%
[28 kg]
non-water

1/3
[14 litres]
Extracellular fluid (ECF)

3/4
[10.5 litres)
Extravascular fluid

1/4
[3.5 litres]
Intravascular fluid

Figure 1

equilibration. This can be avoided by utilizing a method that

mathematically compensates for elimination. This is achieved by
taking serial measurements of plasma concentration once initial
redistribution has occurred in order to infer the rate of elimination. As elimination is typically exponential, the logarithm of
marker concentration, LogC, can be plotted to give a linear
relationship with time (Figure 2). From this, linear regression can
be used to extrapolate the dye concentration before measurements began (and before initial distribution was complete).
The extrapolated concentration at time zero, C0, will represent
the theoretical concentration if even distribution of the marker

occurred instantaneously. As the value for E must be zero,

Equation 1 can be simplified as:
V

The accuracy of this method has been questioned. A common

criticism arises from the variation in estimated ECF volume between different marker compounds. For example, the derived
volume of distribution for inulin is less than that of sodium
bromide. It is suggested that perhaps inulin is so large a molecule
that it cannot reach all interstices of the compartment or that
NaBr is able to permeate the ICF in small quantities. Nonetheless,
each molecule has a house standard distribution volume, deviations from which can then be interpreted.

LogC

Fluid composition
The fluids in the extracellular and intracellular compartments
show marked differences in their ion content. The relative concentrations of the major positive (cations) and negative (anions)
ions can be seen in Figure 3. Overall, in each compartment there
is an equal positive and negative charge. In addition, the total
osmolarity must be equal across plasma and the intracellular
space otherwise, as the cell membrane is freely permeable to
water, osmosis would occur until equilibration is achieved.
The concentrations given in Figure 3 represent plasma water
and the intracellular fluid of myocytes as illustrative examples.
However, it should be noted that due to the differences between
differentiated cell types and their functions, the fluid composition
of the intracellular fluid is highly variable. For example, erythrocytes contain high concentrations of chloride ions and even

Time

Figure 2

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Eq 2

Equation 2. Estimating volume of distribution using serial

measurements of concentration.

Estimating concentration of marker substance, C,

by serial measurement

Equilibrium reached

M
C0

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Ions contributing charge (mEq/kg H 2O ) in intracellular and extracellular fluids

Na+
Ka+
CA2+
MG 2+

CI
HCO 3
Protein
Other

Extracellular fluid
Cations
Anions

Intracellular fluid
Cations
Anions
10

3
7

45
111

159

153
155
27

18
9

4.3
5.4
2.2

40

Figure 3

Fluid balance

this is subject to variation. Red cells contain carbonic anhydrase

allowing carbon dioxide available in the peripheral circulation to
react with water forming bicarbonate and hydrogen ions. As
these are charged moieties, they cannot simply diffuse back out
of the cell. While the protons bind to haemoglobin, an exchange
transporter called Band 3 allows bicarbonate to leave the cell in
exchange for chloride ions. This process, known as the chloride
shift, is then reversed as blood passes through the pulmonary
circulation and is just one example of how variation in ion
concentration can occur.
Differences also exist between the intravascular and interstitial compartments. As considered in the discussion of dilution
measurements, not all solutes will cross the endothelium and
enter interstitial fluid.
The values in Figure 3 demonstrate that the overall total
positive and negative charge in the plasma water is 165 mEq/kg
H2O compared to 210 mEq/kg H2O in the intracellular compartment. The reason for this lies in the relative protein concentration between the two compartments; these polyvalent
intracellular anions contribute a greater charge with only a small
number of particles contributing to osmolarity.

The typical fluid balance for a person undergoing a semisedentary lifestyle is set out in Table 1. As might be expected,
oral intake accounts largely for the input but is supplemented by
the oxidation of compounds to produce carbon dioxide and
water. Urine is the primary output of fluid but a large proportion
is lost through the skin as perspiration and the lungs but due to
reabsorption in the large bowel water content of faeces is relatively low.
It can be appreciated that in even moderate exercise an increase in water loss would occur through the lungs secondary to
hyperventilation and the skin as part of thermoregulation. This
demands an increased intake as well as shifting the relative
contributions of the factors in Table 1.
Administered fluids
The control of fluid balance is self-evidently important. Hypovolaemia results in hypoperfusion which may in turn result in
organ dysfunction. Conversely, hypervolaemia and consequent
oedema may also result in dysfunction. When considering fluid
replacement therapy the property of the infused fluid determines
the distribution of that fluid within and between body compartments. Most patients undergoing general anaesthesia will receive
some form of intravenous (IV) fluid and knowledge of the
mechanisms of fluid distribution is key to successful therapy.

Typical fluid balance in a 70-kg man over 24 hours

Input
Food
Drink
Oxidation
Total

Output
1200 ml
1000 ml
300 ml
2500 ml

Urine
Skin/lungs
Faeces
Total

Dextrose: If 1 litre of dextrose (glucose 5%) is given to a patient,

the glucose will be rapidly metabolized by the liver, leaving pure
water that can freely permeate all fluid compartments. The water
will therefore distribute proportionally to the size of the compartments. Thus, if we consider Figure 1 a third will become ECF
and a twelfth will remain intravascular, contributing around 80

1500 ml
900 ml
100 ml
2500 ml

Table 1

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ml to plasma volume. This can be seen experimentally, as dilution of albumin following dextrose infusion resolves within
1 hour confirming the transient effect on plasma volume.

Clinical examination for changes in skin turgor and capillary

refill time or simply asking the patient about thirst are often cited
as a simple first-line steps in assessing the fluid status of a patient. Non-invasive observations such as blood pressure or heart
rate can be used as indicators of hypovolaemia. However, a
healthy patient can undergo losses up to a quarter of their blood
volume without exhibiting a measurable hypotension or tachycardia owing to innate physiological compensation and reserve.
Although, it has been suggested that measuring for postural
changes in blood pressure can be more revealing. The presence
of pulmonary/peripheral oedema or raised jugular venous pressure on examination can be indicators of hypervolaemia. In the
patient observed over time, fluid balance charts and weight
change can also be interpreted to infer fluid status. However,
these approaches are often unreliable unless a patient lies at the
extremes of fluid imbalance.
Rather than relying on indirect indicators or quantifying
concentrations of variable endogenous compounds, more proactive approaches have been developed. The simple dilution tests
described above may allow a patients volume status to be
measured swiftly and accurately. An alternative approach is the
use of oesophageal Doppler monitoring to measure the blood
flow of the descending aorta from which cardiac stroke volume,
stroke distance and the duration of aortic flow can be measured
or inferred, which is in turn used as an indicator of volume
response. This allows for a much more sensitive fluid challenge
to be performed.
The FrankeStarling curve underpins the approach to fluid
balance, the central aim being to maximize cardiac contractility.
The cardiac output is determined by the intersection of the Frank
eStarling curve and the Guyton curve (Figure 4). The total volume in the arterial and venous circulations determines the mean
circulatory filling pressure, Pmcf. Increasing Pmcf causes a rightward shift of the Guyton curve which, if the patient is hypovolaemic, moves the intersection to a higher point on the Frank
eStarling curve, therefore increasing contractility. Oesophageal
Doppler scanning allows this increase in contractility to be

Normal saline: Normal saline (NaCl 0.9%) is a crystalloid fluid

isotonic to plasma. It is cheap and has been considered to be safe.
However, both sodium and chloride ions are freely filtered in
capillaries (see Anaesthesia & Intensive Care Medicine 2012;
13(11): 573e580) thus the solution would be expected to equilibrate across the entire extracellular compartment. As seen in
Figure 1, only 25% of this represents the intravascular fluid.
Therefore if 1 litre of normal saline is infused intravenously it
would be expected that approximately 250 ml remains as plasma
while the remainder extravasates. Although saline is not seen to
affect serum osmolarity, it is known to produce a metabolic
acidosis through a presumed increase in strong ion difference in
the form of hyperchloraemia. (see Anaesthesia & Intensive Care
Medicine 2012; 13(11): 567e572)
Hartmanns solution: Hartmanns solution or compound sodium lactate (CSL) is another crystalloid fluid that contains a
range of ions in a similar distribution to ECF as shown in
Figure 3. For this reason, it is often considered a more physiological choice than saline administration. As it comprises small
ions, these are freely filtered at the endothelium and so the
volume of distribution will include the interstitium producing the
same approximate contribution to plasma volume as does saline.
Both NaCl and Hartmanns solution show a much slower return
to baseline in protein dilution studies compared to dextrose,
consistent with this assumption.
Colloidal fluids: These contain macromolecules, typically proteins or polysaccharides greater than 35 kDa, such that capillary
endothelia are non-permeant for example 0.4% succinylated
gelatin (Gelofusine), 6% hydroxyethyl starch (Voluven) or 5%
albumin solution are common examples. These large molecules
will remain intravascular thus confining the associated fluid to
this compartment (at least in theory). Therefore if 1 litre of
colloid fluid is administered it would be expected that it
contribute 1 litre to the plasma volume, hence they are often
referred to as plasma expanders. Despite this theoretical targeting
of the fluid to the intravascular space, investigation has revealed
extravasation of substantial quantities of the infused volume.
The degree to which this occurs appears to be specific to the
clinical indication thus the nature of the dehydration must be
considered when planning a fluid regimen. It should also be
considered that specific clinical risks exist with colloids, such as
anaphylaxis, coagulopathy and macromolecule deposition leading to pruritus.

FrankStarling curve for cardiac contractility and

the Guyton venous pressure line
Q

FrankStarling
curve

Indications for fluid administration: The assumption that

large-volume fluid replacement is necessary in all perioperative patients is long-standing and the classical 3 litres/24
hours approach is widely adopted. However, fluid overload is
commonplace and potentially severe consequences such as
hyponatraemia can occur, particularly if inadequate potassium is supplemented. This suggests that greater emphasis
needs to be placed on the individualized assessment of patient
needs.

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Guyton curve

Pmcf

Pv

Figure 4

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observed. Modest fluid boluses can be given until appreciable

increase in stroke volume is no longer seen. At this point it can
be assumed that the patient is at the peak of their FrankeStarling
curve and further volume increase could push them onto the
downward slope.
Randomized controlled trials have indicated that this may
improve outcomes in patients undergoing major surgery. As a
result oesophageal Doppler monitoring is now recommended in
colorectal surgery patients to ensure optimal fluid balance is
attained.
An interesting example to consider is anaesthesia-induced
hypotension, which is a common clinical phenomenon in
epidural and spinal anaesthesia. Blockade of the sympathetic
nervous system input to the vasculature results in vasodilatation.
Dilution methods demonstrate that plasma volume remains unchanged and therefore fluid administration risks volume overload. If we consider the Guyton curve, it has now steepened
rather than shifted, resulting in an increased cardiac output at its
intersection, and thus potential for increased contractility is
limited and the rise in arterial pressure relative to increases in
Pmcf is reduced. Therefore, despite the hypotension, intravenous
fluids may not be an appropriate intervention and the circumstances may instead favour vasopressor therapy.

It is estimated that a 10% change in circulating volume is

required to stimulate thirst through this pathway. Thus the body
is more sensitive to osmotic or intracellular dehydration than it is
to extracellular dehydration. However, it is generally accepted
that these two mechanisms work efficiently in tandem to produce
appropriate volume regulation.
Correction of fluid imbalance
Thirst: Oral fluid intake is driven by thirst in response to hypothalamic signalling, associated with dryness of the mouth and
throat, mediated by a decrease in secretions by the salivary and
buccal glands.
Antidiuretic hormone: A peptide hormone released by the pituitary neurohypophysis known as antidiuretic hormone (ADH),
or arginine vasopressin (AVP), has a key role in water homeostasis. ADH release classically occurs in response to an increase
in plasma osmolality, or a decrease in circulating blood volume.
ADH acts on Type 2 vasopressin (V2) receptors on the basolateral surface of the renal collecting duct epithelium. Through Gs
protein signalling this stimulates the exocytosis of aquaporin
2 (AQP2) containing intracellular vesicles at the apical surface,
incorporating these pores into the membrane, allowing water
molecules to permeate the cell. This facilitates free water reabsorption thus reducing loss in urine and maintaining total body
water. Trauma or surgery can induce release of ADH contributing
to the hormonal injury response and ensuring water retention at
times when it may be physiologically useful.
However, its actions can be best appreciated by considerations of the pathologies in which it is mal-regulated. In the
syndrome of inappropriate ADH secretion (SIADH) water is
reabsorbed to excess resulting in volume overload and potentially severe hyponatraemia. Vaptan drugs are V1/V2 antagonists
that can reverse this effect and have a role in rapid correction of
hyponatraemia by reducing the AQP2 density at the membrane.
An important point here is that fluid restriction is considered the
treatment of choice in such patients and should be thought of as
an efficacious intervention in its own right. Conversely, in diabetes insipidus, the reduced release, or response to, ADH results
in a diuretic effect producing the characteristic polyuria. The
short-term dehydrating effect of ethanol also occurs by inhibition
of ADH release, with a resultant diuresis.

Mechanisms of volume homeostasis

In a healthy individual, total body water does not fluctuate
beyond very tightly controlled limits. Detection of reduced fluid
volume occurs by numerous mechanisms resulting in the
increased intake and decreased loss of water in order to efficiently return the volume to baseline.
Detection of fluid imbalance
Intracellular dehydration: This mechanism is exquisitely sensitive, and has been demonstrated to respond to 1e2% change in
fluid volume. Loss of hypotonic fluids from the extracellular
compartment, for example as perspiration, produces an increase
in the ECF osmotic pressure. This leads water to osmose from the
intracellular compartment to reduce the osmotic gradient. This
effect leads to reduced intracellular volume in osmoreceptor cells
of the circumventricular organs. These specialized cells lack a
bloodebrain barrier allowing them to be sensitive to changes in
plasma osmolarity. These neurons project to magnocellular cells
in the supraoptic and paraventricular nuclei of the hypothalamus
resulting in signalling to the cerebral cortex allowing thirst to be
consciously appreciated. Interestingly, small, uncharged molecules such as urea do not contribute to this osmotic gradient, as
they are able to freely move across the cell membranes, thus their
concentration can increase without giving rise to sensations of
thirst.

Mechanisms of sodium homeostasis

The ionic composition of body fluids in tightly regulated, sodium
as the major extracellular cation is no exception. It is important
to remember that sodium homeostasis is closely related to ECF
volume but also to potassium balance. In a Western diet, normal
salt intake is 6e18 g/day (100e300 mmol). Sodium loss occurs
via the skin, through perspiration, and the gastrointestinal tract,
but the principal site of sodium regulation is the kidney normally
accounting for 95% of sodium output. In a healthy individual
sodium intake and sodium excretion should be approximately
equal over time.
Sodium retention is associated with fluid retention and
oedema, and sodium depletion with shrinkage of the ECF volume
and hypovolaemia. The epithelial sodium channel (ENaC) allows
the reabsorption of sodium at the collecting duct, promoting

Extracellular dehydration: Extracellular mechanisms for the

detection of volume depletion are found in the cardiovascular
system and as such are primarily responsive to changes in the
intravascular volume. These include the arterial baroreceptors in
the carotid sinus and aortic arch, as well as volume receptors in
the cardiac atria and great veins in the thorax and of course the
kidney. These systems are then able to transmit signals to the
hypothalamus also resulting in thirst.

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Sympathetic nervous system activity

Renal sympathetic activity also has an effect on renal blood flow,
as well as directly promoting reabsorption of sodium by the
tubular cells. Perhaps for these reasons, renal sympathetic activity has been implicated as a potential mechanism for essential
hypertension leading to investigation into renal sympathetic
nerve ablation as a potential curative measure.

water reabsorption and therefore anti-diuresis demonstrating the

inter-relation of sodium and volume regulation. The clinical
significance of this is clear to be seen in Liddles disease. A
mutation increases ENaC recycling and therefore produces
upregulation and fluid volume increases associated with early
onset hypertension.
A number of renal mechanisms affect sodium regulation
including glomerular filtration rate (GFR), renal tubular mechanisms, the renineangiotensin axis, sympathetic activity, aldosterone levels, as well as atrial natriuretic peptide (ANP).

Atrial natriuretic peptide (ANP)

ANP is released from cells in the atria in response to stretch
suggesting sensitivity to an increase in blood volume; as might be
expected ANP promotes natriuresis.

Glomerular filtration
An increase in ECF volume leads to an increase in renal perfusion, the filtered volume at the glomerulus, the GFR, and sodium
load presented to the proximal tubule is also increased resulting
in a greater loss of sodium and water. This mechanism is known
as pressure-natriuresis and represents another important entanglement of sodium/volume homeostasis.

Potassium homeostasis
Normal intake of potassium in food is about 100 mmol/day;
around 10% is lost in the faeces and 90% in the urine. Unlike
sodium only negligible quantities of potassium are present in
sweat. As discussed above, aldosterone is released in response to
hyperkalaemia and acts to increase the urinary excretion of potassium. When plasma potassium rises acutely, such as following
major tissue damage, this mechanism stimulates the kidney to
quickly excrete the excess. Furthermore, insulin and catecholamines both stimulate the Na/K-ATPase pump on basolateral
cell membranes, promoting uptake into the cells, producing a fall
in plasma concentration. To combat hypokalaemia, aldosterone
secretion is directly inhibited and potassium excretion by the
collecting duct diminishes.
It is important to recognize that while the nephron can reabsorb sodium, this is only achieved by the concomitant excretion
of potassium or hydrogen to maintain electrochemical balance.
Hence the need for adequate potassium supplementation in fluid
regimens to prevent hyponatraemia discussed above.
A

Glomerulotubular balance
Glomerulotubular balance is a process whereby the proximal
tubule and the loop of Henle increase their rates of sodium
reabsorption in response to decreased GFR so that excess losses
do not occur. For example following haemorrhage, the reduced
filtered sodium load is absorbed more completely.
Renineangiotensinealdosterone system (RAAS)
Renin production by the juxtaglomerular granular cells is sensitive to extracellular osmolarity. Renin is then able to convert
angiotensinogen to angiotensin I, which is further processed by
angiotensin-converting enzyme (ACE) to produce angiotensin II,
which is a powerful vasoconstrictor. Seminal work by Guyton
and Hall in 1980, demonstrated that in normal dogs increased
sodium intake results in increased excretion of sodium within a
tightly regulated mean arterial pressure, Pa. However, when
normal renal mechanisms were disrupted by infusion of angiotensin II or ACE inhibitor captopril, Pa depended markedly on
sodium loading. Angiotensin II also produces an upward shift in
the pressureenatriuresis curve therefore maintaining sodium
homeostasis at the expense of volume regulation. In addition to
this, it is known to act directly on circumventricular neurons to
stimulate ADH secretion and thirst. Finally, angiotensin II stimulates the synthesis and release of aldosterone.

FURTHER READING
Barrett KE, Boitano S, Barman SM, Brooks HL. Ganongs review of medical
physiology. 23rd edn. Lange, 2009.
Hall JE. Guyton and Hall textbook of medical physiology. 13th edn.
Saunders, 2015.
Pocock G, Richards CD, Richards D. Human physiology: the basis of
medicine, (Oxford Core Texts). 4th edn. Oxford University Press, 2013.

Practice points

Aldosterone
Aldosterone is considered the main effector of reabsorption in the
long-term control of sodium balance however its regulation is
complex. Aldosterone secretion is controlled by angiotensin II, ultimately a form of renal control as well as by adrenocorticotropic
hormone released from the pituitary, representing a form of
neuroendocrine control. Furthermore, perfusion of the adrenal
cortex by plasma with low sodium, or high potassium, concentrations stimulates aldosterone secretion directly. Aldosterone increases reabsorption of the filtered sodium through the
mineralocorticoid receptor with actions as a transcription factor.
This results in upregulation of ENaC expression promoting collecting duct permeance to sodium, facilitating its retention. However,
recent work has revealed stimulation of inward currents within 60
seconds of administration suggesting multiple modi operandi.

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Total body water is divided into fluid compartments of differing

volumes and compositions
The measurement of these compartments can be achieved using
dilution methods
When administering intravenous fluids, careful consideration
should be given to how they will distribute across the
compartments
Endogenous mechanisms for detecting fluid imbalance can be
considered as intracellular or extracellular
Renal mechanisms act to reduce water loss while hypothalamic
mechanisms stimulate thirst to encourage increased intake
Sodium balance is controlled primarily by renal mechanisms
Fluid, sodium and potassium balance regulation cannot be
considered individually, they are closely inter-related

2015 Published by Elsevier Ltd.