C O N T I N U I N G P R O F E S S I O N A L D E V E LO P M E N T

Fluid balance

Regulation of water, sodium By reading this article and writing a practice profile, you can gain
and potassium: implications
for practice 36-42 ten continuing education points (CEPs). You have up to a year to
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Practice profile 25

Regulation of water, sodium and

potassium: implications for practice
NS77 Edwards S (2001) Regulation of water, sodium and potassium: implications for
practice. Nursing Standard. 15, 22, 36-42. Date of acceptance: September 29 2000.

the kidneys, gastrointestinal tract, respiratory

Aims and intended learning outcomes
tract and skin. In the healthy adult (Marieb 1998):
The aim of this article is to provide an overview ■ The kidneys excrete approximately 1.5-2l fluid
of the physiology and regulation of water, sodium daily, depending on intake.
in brief and potassium balance in the body, and the asso- ■ Faecal loss amounts to 300ml daily.
ciated implications for practice. Understanding the ■ Losses from the skin and respiratory passages
Author physiological principles involved is important to account for approximately 0.6/1l daily.
Sharon Edwards RGN, DipN, ensure patients’ fluid balance is maintained during
MSc, PCGEA, is Senior and following treatment, to explain incidents that
Lecturer, University of Body fluid compartments
occur in clinical practice and their rationale.
Hertfordshire. After reading this article you should be able to: Table 1 lists the different body fluid compartments.
[Link]@[Link]
■ Understand fluid, sodium and potassium Intracellular fluid (ICF) is defined as all the body
Summary physiology and homeostasis. water within cells. It constitutes about 40 per
Regulation of fluid balance is ■ Indicate the conditions and treatments that influ- cent of total body weight. It is inhomogeneous,
a complex subject. Sharon ence fluid, sodium and potassium physiology. having different pH and ionic composition
Edwards discusses the ■ Demonstrate how fluid regimens and hypergly- depending on the organ or tissue involved.
physiological principles caemia, hyperlipidaemia and hyperproteinaemia Extracellular fluid (ECF) is found outside the cells
involved.
alter fluid, sodium and potassium homeostasis. and is commonly subdivided into plasma and inter-
stitial fluid volumes. It constitutes about 20 per
Keywords cent of total body weight. With acute or chronic
Introduction
■ Anatomy and physiology illness, ICF volume is reduced and ECF volume is
■ Biological sciences To maintain fluid and electrolyte balance, water, increased, and might even exceed ICF volume.
sodium and potassium are in constant motion Plasma, or intravascular fluid, is contained in
These key words are based between the intracellular and extracellular body blood vessels and plasma volume, not including
on subject headings from the compartments (Edwards 1998). the volume of the blood cells. Interstitial fluid, or
British Nursing Index. This Body fluids are complex aqueous solutions, in the third space, is water between the cells and
article has been subject to which biochemically distinct compartments are outside the blood vessels. It is the fluid that accu-
double-blind review. divided by the plasma membrane (between the mulates following burns and soft tissue injuries
intracellular and extracellular compartments) or (Rooney 1995). The transcellular compartment is a
by specialised cell layers (between intravascular, collection of biochemically distinct fluids including
Online archive interstitial and transcellular compartments). Total cerebrospinal, synovial, pleural, pericardial,
body water (TBW) accounts for between 50 per intraocular and peritoneal fluids and digestive
For related articles visit our cent (females) and 60 per cent (males) of an adult’s secretions, which are separated from the intersti-
online archive at: total body weight (Marieb 1998). tial compartment by a layer of epithelium
[Link] The average adult has a normal fluid intake of (Flanning 2000). Transcellular components are
and search using the key 2-2.5l per day from drinks, water in food or from oxi- formed by transport activity of cells. The fluid is
words above. dation of food during metabolism, which produces extracellular and is often considered as part of
200-300ml per day (Rooney 1995). Fluid is lost via the interstitial volume (Worthley 1999).

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Fluid balance

The transcellular compartment is small compared Table 1. Major fluid compartments of the body
to the intravascular, interstitial and intracellular
compartments. However, when larger volumes Total body water volume = 42l, 60 per cent of body weight
occur, such as in diseased states (for example,
bowel obstruction or cirrhosis with ascites), it is Intracellular fluid (ICF) volume Extracellular fluid (ECF) volume
formed at the expense of the remaining intersti- = 28l, 40 per cent of body weight =14l, 20 per cent of body weight
tial and plasma volumes (Worthley 1999).
The extracellular fluid and intracellular fluid con- Interstitial fluid Plasma
tain the major electrolytes, that is, products of Approximate volume and percentage of volume = volume =
ionic compound dissociation in solution. The body weight values are noted for a 70kg 11l, 80% 3l, 20%
concentration of electrolytes is measured in mil- male (Marieb 1998) of ECF of ECF
liequivalents per litre (mEq/l). Cations carry a
positive charge, and anions carry a negative glucose combined with 0.2-0.9% normal saline
charge. The main cation of ECF is sodium, and 25% albumin) have a higher concentration
whereas that of ICF is potassium. The main of osmotically active particles than isotonic solu-
anions of ECF are chloride and bicarbonate, tions (Galbraith et al 1997).
while those of ICF are proteins and organic phos- The concentration of osmotically active solutes
phates. Molecules such as glucose or urea, which in the fluid compartments determines the distri-
are uncharged in solution, are also present. bution of body water. Osmotically active solutes
that cannot move freely between fluid compart-
ments influence the movement of water into
Movement between compartments
and out of that compartment (Flanning 2000).
Several factors contribute to maintaining the dif- Active transport is the movement of particles
ferences in solute composition between ECF and against a concentration gradient. This is provided
ICF. To pass between ECF and ICF, solutes must by transmembrane proteins that require energy
cross the plasma membrane. Some move freely to passively enhance permeability to a given
across the membrane due to concentration dif- substance by providing a channel, or pore, for
ferences, but the majority require some form of easy passage of water-soluble/lipid-insoluble
assistance. Diffusion is the random movement of molecules. An example is the sodium/potassium
particles in all directions from an area of greater pump, which moves sodium from the inside of a
concentration to an area of lesser concentration cell to the outside, where sodium concentration
(Bove 1994). Diffusion depends on: is greater, and returns potassium to the inside of
■ Membrane permeability. the cell, where potassium concentration is
■ The particle’s electrical charge. greater.
■ The pressure gradient around the membrane. Filtration is the movement of water and particles
An example is when sodium moves from the from an area of high pressure to an area of low
outside to the inside of cells because the sodium pressure through a semipermeable membrane,
concentration is higher on the outside. for example, renal glomerular filtration of blood.
Osmosis is the movement of water from a
solution of lesser to a solution of greater solute
Implications for practice
concentration. In osmosis, the membrane is
permeable to water, but only selectively perme- Factors in practice that cause water, sodium and
able to particles (Bove 1994). If, for example, potassium to move abnormally between fluid
pure water in a beaker is separated from a highly compartments are physical conditions (trauma
concentrated water and salt solution by such a and shock, and respiratory acidosis and alkalosis)
membrane, water will flow across the membrane and treatments (blood transfusions, rewarming
into the salt solution. following hypothermia, drugs and insulin).
Osmolality is a measure of the osmotically active Trauma and shock Any type of trauma, shock
particles in solution for a given unit of mass. Isotonic or cell damage (such as surgery, myocardial
solutions have equal concentrations of osmoti- infarction, head injury) will automatically trigger
cally active particles in solution (whole blood, an inflammatory response (Bove 1994).
Hartmann’s solution, 0.18% NaCl in 4% dex- This causes a rapid and proportional increase in
trose, 5% dextrose, and 0.9% saline). Hypotonic capillary permeability, due to the release of
solutions (water, 0.45% normal saline and 4% localised mediators, such as kinins. The permeabil-
glucose) have a lower concentration of osmotically ity causes movement of water, electrolytes and
active particles than isotonic solutions. Hypertonic other particles (such as albumin) into the interstitial
solutions (25% mannitol, 10% glucose, 5-10% spaces to allow the necessary factors to reach the

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Fluid balance

site of injury. This third-space fluid shift (Bove into the cells in exchange for ICF potassium and
1994) leads to localised swelling and lymphatic sodium, increasing the ECF pH. Thus, hyper-
blockage, causing localised interstitial oedema. kalaemia and acidosis often occur together. In
A patient might then appear ‘dry’ or hypo- the event of a respiratory or metabolic alkalosis,
volaemic, having a low circulating blood volume ECF potassium exchanges with ICF hydrogen
as fluid has moved into interstitial spaces, yet the (hypokalaemia) correcting the alkalosis by reduc-
amount of body water might not have changed. ing the pH of the ECF. A metabolic alkalosis
The release of cell mediators causes a reduction enhances renal potassium loss by encouraging
in blood pressure and an increase in heart rate, distal nephron sodium/potassium, in preference
further compounding the appearance of a hypo- to sodium/hydrogen exchange.
volaemic state (Huddleston 1992). This state
stimulates compensatory homeostatic control TIME OUT 1
mechanisms to reabsorb sodium and water and David is 18 and has asthma.
to cause vasoconstriction, in an effort to restore He develops severe breathing
circulating volume and increase blood pressure. difficulties and is admitted to
As a result, venous capacity is decreased to match A&E with an asthma attack. On
admission to your ward his arterial
the smaller blood volume, so that adequate trans-
blood gases from A&E reveal that he has a
port of oxygen and nutrients is maintained.
respiratory alkalosis and laboratory blood
As overfilling of the third space becomes critical, results show that David’s potassium level is low.
the ability of homeostatic mechanisms to com- ■ Explain why his potassium level is low.
pensate reduces: the central venous pressure ■ What is potassium exchanged for in a
(CVP), diastolic filling pressure, stroke volume and respiratory acidosis and why?
systemic arterial blood pressure fall, and oxygen ■ What occurs to the ECF pH during respiratory
diffusion from capillary to cell is impaired, causing alkalosis? What other effects might this have?
hypoxic damage to organs. This process might
predispose a major trauma victim to excessive Blood transfusions When blood is stored, the
stimulation of inflammatory pathways, leading to sodium and potassium concentration alters. A
a severe and prolonged increase in vascular perme- unit of stored blood contains approximately
ability with severe interstitial oedema in capillary 75-80mEq sodium and 5-7mEq potassium
beds remote from the site of injury. The result of (Contreras 1992). Patients with normal cardiac
this is hypovolaemia, which is associated with sys- and renal function will probably be able to handle
temic inflammatory response syndrome (SIRS) the increase in sodium and potassium. However,
(Reilly and Yucha 1994). in patients with severe trauma and shock who
Following injury, potassium moves out of the have cardiac and renal dysfunction, the sodium
cell. In a normal cell, high intracellular potassium and potassium content of stored blood can have
and low intracellular sodium concentration is profound effects. Initiation of homeostatic
maintained by the sodium/potassium pump. The mechanisms to enhance sodium and water
damage of trauma or shock affects the pump reabsorption can promote fluid overload. As a
action, increasing sodium inside cells. This results consequence, diuretic therapy might be given
in water entering cells by osmosis, causing cellular following each unit of blood or every consecu-
swelling and distortion, which might interfere tive unit (Edwards 2000).
with cellular organelle function (Buckman et al
1992). If renal function is sustained, potassium TIME OUT 2
will be excreted and, as cell repair begins, Arthur needs a blood transfusion
hypokalaemia (inadequate levels of potassium in following surgery to repair a
the bloodstream) will develop without an ade- hernia. He has angina, which is
stabilised on drug therapy. During
quate supplement of potassium.
his second unit of blood he feels
Acidosis and alkalosis Cellular uptake of
breathless. The doctor takes a blood sample
potassium is regulated by the sodium/potassium and prescribes frusemide 20mg.
pump, while movement of potassium out of the ■ What might be happening to Arthur during
cell is governed by passive forces (cell membrane this blood transfusion?
permeability and chemical and electrical gradi- ■ What are the consequences of an increased
ents to the potassium ions). sodium and potassium load, bearing in mind
Respiratory or metabolic acidosis promotes a shift Arthur’s heart condition?
of potassium out of the cell, leading to higher than ■ What homeostatic mechanisms might be
normal levels of potassium in the bloodstream allowing Arthur to become breathless?
(hyperkalaemia). In acidosis, hydrogen ions move ■ Why might frusemide have been prescribed?

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Fluid balance

Rewarming following hypothermia When situations. However, prolonged use can result in
rewarming patients following hypothermia, fre- reversal of the hypertonic state to interstitial/
quent estimations of serum potassium should be intracellular, drawing fluid back into the interstitial
made. As the patient’s temperature decreases, space and worsening the oedematous state.
alterations in potassium levels occur due to Digitalis overdose can cause hyperkalaemia by
changes in the sodium/potassium pump inhibiting the sodium/potassium pump, which
(Edwards 1999). This can result in increased ECF maintains high intracellular potassium and high
potassium levels during hypothermia. On re- extracellular sodium. In addition, hypokalaemia
warming, the potassium equilibrium is returned and the administration of digoxin can enhance
to normal and hypokalaemia might follow the efficiency of the drug.
(Fritsch 1995). In the hypothermic patient, a
high blood potassium level is often used as a
Fluid, sodium and potassium homeostasis
predictor of non-survival, particularly for levels
greater than 10mEq/l (Schaller et al 1992). Fluid and electrolyte homeostasis is maintained
Insulin Potassium depletion occurs when insulin by the kidneys, brain, lungs, skin and gastro-
treatment is initiated. Insulin promotes cellular intestinal system. Therefore, if patients have
uptake of potassium, causing a deficit in ECF conditions involving these organs, fluid, sodium
potassium independent of the movement of glu- and potassium balance might be affected.
cose. An insulin regimen of IV dextrose 50g with Movement of water and solutes is influenced by
20 units of soluble insulin, might be used in the complex interaction of regulatory processes,
hyperkalaemia caused by excessive intake, severe receptor responses, enzymes, and hormones.
tissue damage, decreased excretion (such as renal Sodium balance regulates ECF volume and various
failure) or body fluid compartment shift (Worthley hormonal and physical ECF volume sensors
1999). Severe hypokalaemia might occur if insulin control sodium excretion.
is administered without potassium supplements. Mechanisms for maintaining water balance in
Because insulin promotes cellular entry of the body include hypothalamic regulation of
potassium, insulin deficits, which occur with thirst and regulation of renal excretion of water.
conditions such as diabetic ketoacidosis, are Osmoreceptors If concentrations of sodium are
accompanied by hyperkalaemia. Potassium increased, as in the case when there is a loss of
homeostasis is not possible in the absence of extracellular water (Bove 1994), osmoreceptors in
renal function (Flanning 2000), when an the hypothalamus are stimulated. Osmoreceptors
increase in serum potassium will eventually lead are highly specialised hypothalamic neurones
to the need for haemodialysis. that continually monitor the solute concentration
Drugs Beta2 adrenergic agonists (such as salbu- (and thus water concentration) of the blood.
tamol and terbutaline) promote cellular uptake When solutes threaten to become too concen-
of potassium (hypokalaemia), whereas alpha- trated, as in conditions that cause an increased
adrenergic agonists (such as clonidine and its sodium concentration (excessive sweating,
derivative apraclonidine) cause a shift of potassium inadequate fluid intake, burns), osmoreceptors
from the ICF to the ECF (hyperkalaemia). transmit impulses to the hypothalamic neu-
Potassium-sparing diuretics (such as spironolac- rones that synthesise and release anti-diuretic
tone) inhibit sodium reabsorption and potassium hormone (ADH).
and hydrogen secretion by the distal tubule and The secretion of ADH from the pituitary gland
might contribute to hyperkalaemia. However, is initiated by an increase in plasma osmolality or
these diuretics are used in combination with a decrease in circulating blood volume and/or a
diuretics that cause potassium wasting in an lowered blood pressure. An increase in plasma
attempt to balance renal potassium gains and osmolality occurs with a deficit of water or an
losses (Galbraith et al 1997). excess of sodium in relation to water, resulting in
Osmotic diuretics interfere with osmosis; they a decreased extracellular and interstitial fluid
tend to stay in the blood and increase osmolality. volume. The primary stimulus for release of ADH
These diuretics are useful in the treatment of is elevation of plasma osmolality. A secondary
oedematous states, such as glaucoma and ele- stimulus is depletion of plasma volume and the
vation of intracranial pressure (Galbraith et al stress response.
1997). In the presence of mannitol in the ECF, ADH inhibits or prevents urine formation by
fluid in the interstitial space will pass from this increasing the permeability of renal tubular cells to
area into the hypertonic (mannitol-containing) water. Water is then reabsorbed from the distal
blood and to the kidneys for removal. Osmotic tubules and collecting ducts of the kidney and
diuretics act quickly and are useful in emergency returned to the circulation. As a result, less urine is

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Fluid balance

produced, urine concentration increases and thirst excretion through mechanisms similar to those
is aroused. The reabsorbed water decreases plasma which result in sodium retention. Stimulation of
osmolality, returning it to normal. Blood volume aldosterone release occurs following an increase
also increases, thereby improving venous return to in plasma potassium levels, which increases intra-
the heart, cardiac output, and blood pressure. cellular concentrations of potassium ions.
Thirst is experienced when water loss equals Atrial natriuretic peptide (ANP) ANP is pro-
2 per cent of body weight (about 700ml) or when duced by the atrial muscle of the heart in
there is an increase in osmolality. Dry mouth, response to overstretching of the atria wall. Its
hyperosmolality, and plasma volume depletion function is renal elimination of sodium to control
activate the osmoreceptors. The action of sodium and water balance. It also increases
osmoreceptors then causes thirst. glomerular filtration rate and inhibits aldos-
Baroreceptors Baroreceptors are specialised terone production and secretion.
nerve endings that are sensitive to changes in Blood urea nitrogen (BUN) creatinine ratio
volume and pressure. They respond to any BUN reflects changes in urine concentration
decrease in arterial blood pressure, whether it is based on serum levels of urea and creatinine.
due to haemorrhage, peripheral blood pooling, Fever, sepsis, steroid administration, burns and
or a decrease in myocardial contractility. With excessive muscle activity (such as seizures)
decreased arterial pressure or volume depletion, increase BUN levels because of increased protein
such as dehydration from vomiting, diarrhoea, or metabolism or dehydration associated with these
excessive sweating, baroreceptors stimulate the problems. The increased BUN causes the kidneys
release of ADH from the pituitary gland. The to increase sodium and water reabsorption in an
reabsorption of water mediated by ADH then attempt to dilute the concentration of urea and
promotes the restoration of plasma volume. creatinine and maintain circulating volume. The
urine becomes more concentrated. As the stimu-
lating factor improves, the kidneys resume normal
Regulation of sodium and potassium
urea excretion. The protective mechanisms
Sodium balance is achieved by the interaction of described above will cease to function within a
a number of neurohormonal systems which short space of time and circulatory failure will
influence renal reabsorption or excretion of ensue. If treatment is not instigated, a metabolic
sodium. The regulation of potassium is closely acidosis, circulatory failure or progressive shock
tied to that of sodium. will occur in a short space of time.
Renin-angiotensin-aldosterone system The
kidneys have a complex role in restoring ECF vol-
Implications for practice
ume and increasing systemic blood pressure.
This set of interlinked processes involves the The practical application of the factors that control
renin-angiotensin-alderosterone system. This fluid, sodium and potassium homeostasis are fluid
system is stimulated principally when there is a regimens and hyperglycaemia, hyperlipidaemia
decrease in blood pressure. A decrease in kidney and proteinaemia. Prescribed fluid regimens need
perfusion activates the mechanism. Renin splits to be carefully thought out, to prevent severe fluid
angiotensinogen, a substrate present in plasma, and electrolyte disturbances. In addition, if they
into angiotensin. This acts as a vasoconstrictor, are not administered accurately and documented
and stimulates the release of aldosterone. over the stated period, fluid overload and oedema
Aldosterone is a steroid hormone synthesised might ensue.
and secreted from the adrenal cortex. Its release Hyponatraemia develops when serum sodium
is influenced by circulating blood volume and concentration decreases to below 135mEq/l.
plasma concentration of sodium and potassium Hyponatraemia is caused by a sodium deficit or
(when sodium levels are depressed or potassium water excess, leading to an intracellular over-
levels are increased). Its action is to increase hydration. This can occur in fluid regimens
sodium reabsorption in the renal tubules. where fluid loss is replaced with excess intra-
Because water follows sodium, there is a subse- venous 5% dextrose in water. When the body is
quent increase in intravascular volume, resulting functioning normally, it is almost impossible to
in increased venous return to the heart, increased produce an excess of fluid by administering 5%
cardiac output and increased blood pressure. In dextrose. In situations when large amounts of fluid
exchange for sodium, potassium is excreted by are given, the haemodilution (hypo-osmolality) that
the distal tubule of the kidney. Addison’s disease occurs will stimulate osmoreceptors. There will be
results in decreased production and secretion of a reduction in ADH release, resulting in an increase
aldosterone. Aldosterone enhances potassium in urinary output, and excess fluid will be lost.

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Fluid balance

TIME OUT 3 Even though 0.9% saline is often classified as Answers to Time Out 1 and 2
Jack has been admitted for an isotonic solution (Rooney 1995), it does con- TIME OUT 1. David
dehydration. He lives alone tain a higher concentration of sodium (154mEq/l) ■ David’s potassium level is
and sometimes forgets to drink. than plasma (140mEq/l). It should not be used low because he has a
A urine test reveals a specific for maintenance as it contains too much sodium respiratory alkalosis due to his
gravity (SG) of 1035. He is thirsty, for such a regimen, but must be alternated in asthma, and ECF potassium
gaunt and his skin is frail and thin. He is will exchange with ICF
some way with 5% dextrose (Rooney 1995).
administered 5% dextrose and encouraged to hydrogen (hypokalaemia)
This is because sodium is the principal extra-
drink clear fluids, but is given no electrolytes. and correct the alkalosis by
cellular electrolyte, and the solution when reducing the pH of the ECF
The dextrose restores Jack’s urine SG to normal,
infused is distributed only in the ECF, so a primary ■ Potassium moves subscript
his urine output is good, and the nursing staff
increase in extracellular sodium causes an into the cell in exchange for
assume he is no longer dehydrated. However,
Jack’s fluid regimen continues to prescribe 5% osmotic attraction of water and intracellular hydrogen to maintain plasma
dextrose. dehydration. acid-base balance
■ What might be the result of only giving In addition, large infusions of 0.9% saline ■ During a respiratory alkalosis,
Jack 5% dextrose for dehydration? might, because of the high concentration of the ECF pH increases,
■ What normal homeostatic mechanisms sodium, increase blood osmolality so resulting in which affects the oxygen
might be stimulated in this instance? a further load onto the circulation due to the disassociation curve. Less
■ What extra fluid might be required? oxygen is released to the
response of compensatory mechanisms. These
cells
processes cause movement of water to the ECF
Fluid regimens should include 0.9% saline, but if and signs of fluid overload might be evident, with TIME OUT 2. Arthur
so much fluid is administered haemodilution weight gain, pallor, breathlessness, convulsions ■ The increased sodium and
could result, causing complications. It might be and pulmonary oedema being the most obvious. potassium contained in the
necessary to administer a blood transfusion if Although 0.9% saline is much better than 5% blood are having serious
haemoglobin becomes so diluted. Other causes dextrose (which causes water retention and dilu- effects on Arthur due to his
of sodium deficits or water excess are: tional hyponatraemia if infused in excess) for heart condition
■ Inadequate sodium intake or diuretic therapy. resuscitation and operative purposes (that is, ■ The increased sodium level
■ Excessive sweating, stimulating thirst and intake correction of hypovolaemia or hypotension), it is would initiate homeostatic
of a lot of water, which dilutes ECF sodium. still not ideal. Other causes of hypernatraemia are: control mechanisms via the
osmoreceptors to enhance
■ Vomiting, diarrhoea, gastrointestinal suctioning ■ Water depletion, excess sodium and water loss.
sodium and water
or burns. ■ General fever or that caused by respiratory infec-
reabsorption, and if cardiac
When there is a sodium deficit, the ECF exhibits tions that increase respiratory rate, enhance output dropped, the renin-
hypo-osmolality and water moves into the cell, water loss from the lungs and sweating. angiotensin-aldosterone
where the electrolyte concentration is greater. The ■ Diabetes insipidus. system would further
plasma volume then decreases, leading to symp- ■ Diabetes mellitus. promote sodium and water
toms of hypovolaemia. When there is an excess of ■ Polyurea. reabsorption to maintain
water, the ICF and the ECF volumes increase, caus- ■ Diarrhoea which can cause water loss in relation cardiac output. This can
ing symptoms of hypervolaemia or fluid overload. to sodium. promote fluid overload. In
Hypernatraemia is defined as a serum sodium level ■ Insufficient water intake, particularly in patients addition, baroreceptors
greater than 145mEq/l. Excessive serum sodium who are comatose, confused or immobilised. cause vasoconstriction,
increasing blood pressure
can be caused by an acute gain in sodium or a ■ Oversecretion of aldosterone as in primary
and the risk of fluid
loss of water. It is always associated with hyper- hyperaldosteronism, or Cushing’s syndrome,
overload and heart failure
osmolality. The main cause of high sodium levels caused by excess secretion of adrenocorti- ■ Breathlessness is due to left
occurs with inappropriate administration of saline cotropic hormone (ACTH). ventricular failure increasing
solutions (as sodium bicarbonate for treatment of Fluid overload When excess fluid is administered the pressure through the
acidosis during cardiac arrest, or sodium chloride). to patients with acute renal failure, heart condi- lungs, causing cell damage
tions, hypertension, cirrhosis or other conditions, and third-space fluid shift,
TIME OUT 4 this can precipitate a water excess, and there is a which leads to pulmonary
Olivia has had a cardiac arrest. risk of fluid overload. It is most commonly the oedema
Paramedics arrived promptly; result of an excessive administration of a combina- ■ To prevent fluid overload
she was successfully resuscitated tion of intravenous fluids, culminating in an over- and/or cardiac failure,
and given 0.9% saline to diuretic therapy (frusemide)
load of salt and water.
maintain circulating volume and is often given following
If fluid administration is allowed to continue
blood pressure. On admission to A&E, she has each unit of blood or every
unchecked, the neck veins might distend, with consecutive unit
slight difficulty in breathing and is very thirsty.
the increased blood pressure leading to oedema
■ Why is fluid therapy necessary for Olivia?
■ What are the homeostatic mechanisms that formation. If the circulating volume is great
have been stimulated to cause Olivia’s thirst? enough, pulmonary oedema and heart failure can
develop. If cardiac output is allowed to fall, a

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Fluid balance

Answers to Time Out 3 and 4 reduction in renal blood flow will stimulate the mechanisms can no longer maintain intracellular,
TIME OUT 3. Jack renin-angiotensin-aldosterone mechanism, result- extracellular or interstitial fluid, sodium and
■ Jack has a sodium deficit, ing in increased reabsorption of water and salt. potassium disequilibrium ensues. The nurse’s
which leads to intracellular In addition, if circulatory stasis occurs, osmorecep- role in relation to assessment and monitoring of
overhydration and tors will stimulate the release of ADH, reabsorbing fluid and electrolyte balance is well established. A
haemodilution more water and further reducing urine output. The number of patients that require fluid regimens
■ In this situation, the reduction
renin-angiotensin-aldosterone and osmoreceptor have conditions or require other treatments that
in sodium in relation to fluid
mechanisms can lead to circulatory collapse, interfere with or affect their equilibrium of fluid,
in the ECF stimulates
osmoreceptors, reducing the whereby the left side of the heart becomes dys- sodium and potassium balance and/or stimulate
release of ADH from the functional with the consequence of the heart homeostatic control mechanisms. Therefore,
pituitary gland. An increase becoming unable to pump the blood around the nurses need to understand and observe patients’
in urinary output will result body (Edwards 2000). These mechanisms, fluid sodium and potassium levels.
and the excess fluid will be despite attempting to protect the body, actually The extent of this nursing contribution to multi-
lost increase circulating volume and exacerbate the disciplinary care is so far virtually unexplored.
■ Fluid regimen, although symptoms of fluid overload. Future practice with respect to fluid and elec-
prescribed by doctors, Oedema Oedema is the accumulation of fluid trolyte balance might extend beyond assessment,
should alternate with 0.9% within interstitial spaces. This fluid is not available monitoring and securing vascular access for
saline (overload) and 5%
for metabolic processes. A state of dehydration intravenous fluid administration, towards nurse
dextrose (haemodilution) to
can develop as a result of the sequestering of the prescription of intravenous fluids
maintain effective fluid and
electrolyte balance oedematous fluid and in some conditions oedema
and dehydration might be observed. Oedema is TIME OUT 5
TIME OUT 4. Olivia a problem of fluid distribution and does not Now that you have
■ Fluid therapy is necessary to necessarily indicate an excess of fluid. The most completed the article, you
counterbalance the common mechanisms include: might like to think about
third-space fluid shift that ■ Increased hydrostatic pressure (hypertension, LVF). writing a practice profile.
occurs due to cell damage ■ A lack of plasma electrolytes (malnutrition). Guidelines to help you write and
and injury and to prevent submit a profile are outlined on page 44.
■ Increased capillary membrane permeability
the relative hypovolaemia (trauma, injury, surgery).
that might occur
■ Lymphatic obstruction (cancer).
■ A higher concentration of
The accumulation of fluid increases the distance
sodium (154mEq/l) is
contained in 0.9% saline required for nutrients and waste to move
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hypovolaemia and shock. Trauma Quarterly. 8, 4, 12-27.
only in the ECF, causing a infection and formation of pressure sores Contreras M (1992) ABC of Transfusion. Second edition.
primary increase in increase. Oedema of specific organs, such as the London, BMJ Publishing.
extracellular sodium which brain, lung, or larynx, can be life-threatening. Edwards SL (2000) Fluid overload and monitoring indices.
causes an osmotic attraction Professional Nurse. 15, 9, 568-572.
Hyperglycaemia, hyperlipidaemia, hyper- Edwards SL (1999) Hypothermia. Professional Nurse. 14, 4,
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dehydration. In addition, Edwards SL (1998) Hypovolaemia: pathophysiology and
osmolality and attracts water from the cells.
because of the high management options. Nursing in Critical Care. 3, 2, 73-82.
Increases in plasma lipids and proteins displace
concentration of sodium in Flanning H (2000) Fluid and electrolyte balance. In Manley
the ECF, there is an increase water volume and decrease sodium concentration. K, Bellman L (Eds) Surgical Nursing: Advancing Practice.
The osmotic fluid shift to the ECF in turn dilutes the Edinburgh, Churchill Livingstone.
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(stimulating osmoreceptors, concentration of sodium and other electrolytes. Clinical Issues. 6, 2, 196-211.
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resulting in a further load on increased amounts of impermeable solutes causing Edinburgh, Addison Wesley Longman.
Huddleston V (1992) Multisystem Organ Failure:
the circulation a shift of water from the ICF to the ECF to provide Pathophysiology and Clinical Implications. St Louis MO,
osmotic equilibration, thus diluting the ECF sodium. Mosby.
Such resultant hyponatraemia is often associated Marieb EN (1998) Human anatomy and physiology. Fourth
edition. Redwood City, The Benjamin/Cummings
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Reilly E, Yucha CB (1994) Multiple organ failure syndrome.
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Schaller MD et al (1992) Hyperkalaemia: a prognostic factor
A complex interplay of physiological control during acute severe hypothermia. Journal of the
systems maintains fluid, sodium and potassium American Medical Association. 264, 14, 1842-1845.
Worthley LIG (1999) Fluid and electrolyte therapy. In Oh TE
homeostasis. When the activity of the physiolog- (Ed) Intensive Care Manual. Fourth edition. Hong Kong,
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