Fluids final 14.2.14

Water distribution
Water accounts for approximately ;
• 60% of body weight in men.
• 55% in women,
• reflecting the typically greater body fat content in
women.
• Reflection of body fat – lean tissues(muscle, solid
organs) have high water content
• Highest in newborns ~80%

• Approximately 66% of this water is in the
intracellular fluid (ICF)
• While 33% in the extracellular fluid (ECF);
• Only 8% of body water is in the plasma

Fluid Compartments
Intracellular fluid (ICF)
• Fluid inside the cell
• Most (2/3) of the body’s
H20 is in the ICF.
Extracellular Fluid
(ECF)
• Fluid outside the cell.
• 1/3 of body’s H20
• More prone to loss
• 3 types:
Interstitial- fluid
around/between cells
Intravascular- (plasma)
fluid in blood vessels
Transcellular –CSF,
Synovial fluid etc

• Water is not actively transported in the body.
• It is, in general, freely permeable through the
ICF and ECF .
• But its distribution is determined by the
osmotic contents of these compartments.

• Except in the kidneys, the osmotic
concentrations, or osmolalities, of these
compartments are always equal: they are isotonic.
• Any change in the solute content of a
compartment engenders a shift of water, which
restores isotonicity.

• The major contributors to the osmolality of the
ECF ;
• sodium and its associated anions,
• mainly chloride and
• Bicarbonate
• The ICF, the predominant cation is potassium.
• Other determinants of ECF osmolality include;
• glucose
• urea.
• Protein makes a numerically small contribution of
approximately 0.5%.

• This is because osmolality is dependent on the
molar concentrations of solutes: although the total
concentration of plasma proteins is approximately
70 g/L, their high molecular weight results in
their combined molar concentrations being <1
mmol/L.

• However, since the capillary endothelium is
relatively impermeable to protein and since the
protein concentration of interstitial fluid is much
less than that of plasma,
• Therefore the osmotic effect of proteins is an
important factor in determining water distribution
between these two compartments.
• The contribution of proteins to the osmotic
pressure of plasma is known as the colloid
osmotic pressure or oncotic pressure.

• Under normal circumstances,
• the amounts of water taken into the body and
• lost from it are equal over a period of time.
• Water is obtained from the diet oxidative
metabolism.

• The minimum volume of urine necessary for
normal excretion of waste products is about 500
mL/24 h.
• But, as a result of obligatory losses by other
routes, the minimum daily water intake necessary
for the maintenance of water balance is
approximately 1100 mL.

• This increases if losses are abnormally large e.g
excessive sweating diarrhoea.
• Water intake is usually considerably greater than
this minimum requirement but the excess is easily
excreted through the kidneys.
• Water is lost through the
• kidneys,
• skin,
• lungs
• gut

Mechanisms of
Fluid Gain and Loss
Gain
• Fluid intake 1500ml
• Food intake 1000ml
• Oxidation of nutrients
300ml
(10ml of H20 per 100
Kcal)
Loss
• “Sensible”
Can be seen.
Urine 1500ml
Sweat 100ml
• “Insensible”
Not visible.
Skin (evaporation)
500ml
Lungs 400ml
Feces 200ml

Daily Water Gain and Loss
Copyright 2009, John Wiley & Sons, Inc.

Sodium distribution
• The body of an adult man contains approximately
4000 mmol of sodium, 70% of which is freely
exchangeable.
• The remainder being complexed in bone.
• The majority of the exchangeable sodium is
extracellular.
• Normal ECF sodium concentration is 135-145
mmol/L, while that of the ICF is only 4-10 mmol/L.

Sodium distribution
• Most cell membranes are relatively impermeable
to sodium but some leakage into cells occurs and
the gradient is maintained by
• active pumping of sodium from the ICF to the
ECF by Na+, K+-ATPase.

• As with water, sodium input and output normally
are balanced.
• The normal intake of sodium in the western world
is 100-200 mmol/24 h.
• but the obligatory sodium loss, via the kidneys,
skin and gut, is <20 mmol/24 h.

• Thus, the sodium intake necessary to maintain
sodium balance is much less than the normal
intake.
• Excess sodium is excreted in the urine.
• Despite this, excessive sodium intake may be
harmful: there is evidence that it is a
contributory factor in hypertension.

Potassium distribution
• Potassium is the predominant intracellular
cation.
• Some 90% of the total body potassium is free and
therefore exchangeable.
• While the remainder is bound in red blood cells,
bone and brain tissue.

Potassium distribution
• However, only approximately 2% (50-60 mmol)
of the total is located in the extracellular
compartment.
• where it is readily accessible for measurement.
• Plasma potassium concentration is not, therefore,
an accurate index of total body potassium status,
but, because of the effect of potassium on
membrane excitability, is important in its own
right.

water and Sodium
Homoeostasis
• Any loss of water from the ECF, such as occurs
with water deprivation,
• will increase its osmolality and
• result in movement of water
• from the ICF to the ECF.

Water and Sodium
Homoeostasis
• However, a slight increase in ECF osmolality will
still occur,
• stimulating the hypothalamic thirst centre, which
promotes a desire to drink, and
• the hypothalamic osmoreceptors, which causes the
release of vasopressin (antidiuretic hormone or
ADH).

• If ECF osmolality falls, there is no sensation of
thirst and vasopressin secretion is inhibited.
• A dilute urine is produced, allowing water loss and
restoration of ECF osmolality to normal.
• If an increase in ECF osmolality occurs as a result
of the presence of a solute such as urea that diffuses
readily across cell membranes, ICF osmolality is
also increased and osmoreceptors are not
stimulated.

• The vasopressin responses to changes in
osmolality occur rapidly.
• In health, the ingestion of water surplus to
requirements leads to a rapid diuresis.
• And water depletion to a rapid increase in
the concentration of the urine.

Role of Aldosterone
• Aldosterone, released from the adrenal cortex in
response to activation of the renin-angiotensin
system, stimulates
• Sodium reabsorption in the distal parts of the distal
convoluted tubules and collecting ducts
• And is the major factor controlling renal sodium
excretion.

Role of Aldosterone
• But in essence, renin secretion is stimulated
primarily by
• a decrease in renal perfusion secondary to a
decrease in blood volume - specifically by a fall in
arterial blood volume

Natriuretic peptide hormones
• Natriuretic peptide hormones also have a role
in controlling sodium excretion.
• Atrial natriuretic peptide (ANP) is a 28 amino
acid peptide, one of a family of similar peptides,
secreted by the cardiac atria in response to atrial
stretch following a rise in atrial pressure (e.g. due
to ECF volume expansion).

• ANP acts both directly by ;
• inhibiting distal tubular sodium reabsorption
• And through decreasing renin (and hence
aldosterone) secretion.
• It also antagonizes the pressor effects of
noradrenaline (norepinephrine) and angiotensin II
(and thus tends to increase GFR) and has a
systemic vasodilatory effect.

• It appears to provide 'fine tuning' of sodium
homoeostasis but is probably more important in
pathological states than physiologically

Volume Control
• Osmoreceptors and Baroreceptors
– Osmoreceptors in paraventricular and
supraventricular nuclei in hypothalamus –
control thirst and ADH secretion from posterior
pituitary
•Increased free water or decreased osmolality
= decreased ADH and water reabsorption
•Fine tuning day-to-day

Volume Control
– Baroreceptors in cardiac atrium, aortic arch and
carotid sinuses
•Neural and hormonal feedback.

Volume Control
• Renin-Angiotensin
• Renin: released from juxtaglomerular cells of
afferent arterioles in kidney ( BP, NaCl)
• Cleaves angiotensinogen (α-2 globulin
produced by liver) to angiotensin 1

Volume Control
• Angiotensin: cleaved by ACE which is
produced by vascular endothelial cells of
pulmonary tissues.
• Increases vascular tone, stimulates
catecholamine release from adrenal medulla and
sympathetic nerve terminals.
• Decreases RBF and GFR – increases sodium
reabsorption by indirect and direct effect
(aldosterone release from adrenal cortex)

Volume Control
• Aldosterone
• Produced in zona glomerulosa of adrenal
cortex
• Increased absorption of sodium in Collecting
Duct & Distal Convoluted Tubules–
stabilizing Na channel in open state, increases
number of channels in apical membrane
• Increases Na/K activity
• Increases sodium reabsorption and potassium
excretion

Volume Control
• Natriuretic Peptide
– Brain and Renal
•Released by atrial myocytes from wall
distension
•Inhibitory effect on renal sodium absorption
•Urodilatin – ANP-like substance, synthesized by
cortical collecting tubule
–Released by kidney tubules in response to
atrial distension and sodium loading
Twice as potent as ANP, increases cGMP
= Na, Cl, water diuresis

• Physiological responses to a decrease in
plasma volume.
• These involve both responses to restore plasma
volume and maintain blood pressure

Water and Sodium Depletion
• Water depletion or combined water and sodium
depletion will occur if losses are greater than
intake.
• Depletion of water alone is seen much less
frequently than depletion of both water and
sodium.
• As sodium cannot be excreted from the body
without water, sodium loss never occurs alone but
is always accompanied by some loss of water

Water and Sodium Depletion
• Death: Occurs when water loss amounts to
approx
• 15 per cent of body wt. (about 22% of total
body water),
• which happens on about the 7th to 10th day of
complete water deprivation , if not treated.

Water excess
• This is usually related to an impairment of water
excretion.
• However, the limit to the ability of the healthy
kidneys to excrete water is about 20 mL/min
and, occasionally, excessive intake is alone
sufficient to cause water intoxication.
• This can sometimes occur in patients with
psychiatric disorders.

Water excess
• It has also been described in people drinking
large amounts of beer with a low solute content.
• Because this results in a low osmotic load for
excretion and there is a minimum osmolality
below which the urine can not be diluted further.

Water excess
• Increased thirst can occur in ;
• organic brain disease (particularly trauma, and
following surgery).
• Although decreased thirst is more common.

• The clinical features of water overload are
related to cerebral over-hydration, the incidence
and severity depending upon the extent of the
water excess and its time course

Electrolytes of plasma
• Cations mEq/L (a)
Plasma
• Na+ = 143
• K+ = 5
• Ca++ = 5
• Mg++ = 2
• Total = 155
• Anions mEq/L
• Cl– = 103
• HCO–
3 = 27
• HPO-
4 = 2
• SO-
4 = 1
• Proteins– = 16
• Organic acids– = 6
• Total = 155

Electrolytes
• Work with fluids to keep the body healthy and in
balance
• They are solutes that are found in various
concentrations and measured in terms of
milliequivalent (mEq) units
• Can be negatively charged (anions) or positively
charged (cations)
• For homeostasis body needs:
Total body ANIONS = Total body CATIONS

Electrolytes
Cations
Positively charged
 Sodium Na+
 Potassium K+
 Calcium Ca++
 Magnesium Mg++
Anions
Negatively charged
• Chloride Cl-
• Phosphate PO4-
• Bicarbonate HCO3-

Electrolyte Functions
• Regulate water distribution
• Muscle contraction
• Nerve impulse transmission
• Blood clotting
• Regulate enzyme reactions (ATP)
• Regulate acid-base balance

Sodium Na+
• 135-145mEq/L
• Major Cation
• Chief electrolyte of the ECF
• Regulates volume of body fluids
• Needed for nerve impulse & muscle fiber
transmission (Na/K pump)
• Regulated by kidneys/ hormones

Hypernatremia or Sodium excess
• Serum Na+ > 145mEq/L
• Results from Na+ gained in excess of H2O OR
Water is lost in excess of Na+
• Water shifts from cells to ECF
• S/S: thirst,
• dry mucous membranes & lips,
• oliguria,
• increased temp & pulse, flushed skin, confusion
• Tx: IV therapy/diet

Sodium excess
• Sodium excess can result from increased
intake or decreased excretion.
• The clinical features are related primarily to
expansion of ECF volume.
• Sodium overload is more usually due to
impaired excretion than to excessive intake.
• The most frequent cause is secondary
aldosteronism.

Sodium excess
• Secondary hyperaldosteronism ,also known
as
• hyperreninism, or
• hyperreninemic hyperaldosteronism)
• It is due to over-activity of the renin-
angiotensin system.

Sodium excess
• Secondary refers to an abnormality that indirectly
results in pathology through a predictable
physiologic pathway, i.e.,
• a renin-producing tumor leads to increased
aldosterone
• As the body's aldosterone production is normally
regulated by renin levels

Hypernatremia
– Plasma Na+ > 145 mEq / L
– Due to ↑ Na + or ↓ water
– Water moves from ICF → ECF
– Cells dehydrate
Due to:
– Excess Na intake (hypertonic IV solution)
– Excess Na retention (oversecretion of aldosterone)
– Loss of pure water
• Long term sweating with chronic fever
• Respiratory infection → water vapor loss
• Diabetes (mellitus or insipidus) – polyuria
– Insufficient intake of water (hypodipsia)

68
Clinical manifestations
of Hypernatremia
• Thirst
• Lethargy
• Irritability
• Seizures
• Fever
• Oliguria

Hypernatremia
Evaluation
• Volume
• Serum sodium, osmolality, BUN/Creatinine
• Urine sodium, osmolality

Sodium excess
• This is seen in patients who, despite clinical
evidence of increased ECF volume (e.g.
peripheral oedema), appear to have a decreased
effective arterial blood volume,
• Due, for example, to venous pooling or a
disturbance in the normal distribution of ECF
between the vascular and extravascular
compartments.

Sodium excess
• This phenomenon is particularly associated with
cardiac failure, hypoalbuminaemia and hepatic
cirrhosis.
• Many such patients with sodium excess are,
paradoxically, hyponatraemic, implying the
coexistence of a defect in free water excretion.

Sodium excess
• This is probably in part due to an increase in
vasopressin secretion as a result of the decreased
effective blood volume.
• Also, the decrease in GFR and consequent
increase in proximal tubular sodium reabsorption
decreases the delivery of sodium and chloride to
the loops of Henle and distal convoluted tubules.

Sodium excess
• This reduces the kidneys' diluting capacity,
thereby compromising water excretion.
• Renal disease is a relatively uncommon cause of
sodium excess, as is increased mineralocorticoid
secretion due to primary adrenal disease (as in
Conn's syndrome).

Let’s think about….
Hypernatremia
• What are some medical conditions that may cause
elevated serum Na?
• Renal failure
• Diabetes Insipidus
• Diabetes Mellitus ( hyperglycemic dehydration)
• Cushings syndrome (hyperaldosteronism)

Hypernatremia
• What are some other patient populations at risk for
hypernatremia?
• Elderly ( decreased thirst mechanism )
• Patient’s receiving:
-tube feedings
-corticosteroid drugs
-certain diuretic therapies

Hypernatremia
• Sign & Symptoms
• Seizures,
• coma,
• death my result if hypernatremia is left untreated.
• Why?
• Cells loose fluid into the ECF causing irreversible
cell damage.

Sodium measurement
• Sodium concentration used to be measured by
flame photometry, which determines the number
of sodium atoms in a defined volume of solution.
• Sodium is now usually measured by ion-selective
electrodes, which determine the activity of
sodium, that is, the number of atoms that act as
true ions in a defined volume of water.

Hyponatremia
• Serum Na+ <135mEq/L
• Results from excess of water or loss of Na+
• Water shifts from ECF into cells
• S/S: abd cramps, confusion,
• Nausea/Vomiting,
• Headach, pitting edema over sternum
• Rx: Diet/IV therapy/fluid restrictions

Hyponatraemia
• A slightly low plasma sodium concentration is a
frequent finding.
• The mean plasma sodium concentration of
hospital inpatients is 5 mmol/L lower than in
healthy controls.
• Mild hyponatraemia is seen with a wide variety
of illnesses and may be multifactorial in origin.

Hyponatraemia
• It is essentially a secondary phenomenon that
merely reflects the presence of disease
•
• Treatment should be directed at the underlying
cause and not at the hyponatraemia.

Hyponatraemia
• Hyponatraemia itself may warrant primary
treatment
• But usually only when it is severe or associated
with clinical features of water intoxication.

Causes
• It has been emphasized that plasma sodium
concentration depends upon the
• amounts of both sodium and water in the plasma
• Therefore a low sodium concentration does not
necessarily imply sodium depletion.

Causes
• Indeed, hyponatraemia is more frequently a result
of a defect in water homoeostasis that causes
• water retention and
• hence dilution of plasma sodium.

Causes
• One of three mechanisms is usually primarily
responsible for the development and maintenance
of hyponatraemia, although in individual patients
more than one factor may be involved.
• These are:
• 1.Depletion of sodium (hypovolaemic
hyponatraemia)
• 2.Excess of water (euvolaemic hyponatraemia)
• 3.Excess of water and sodium (hypervolaemic
hyponatraemia).

Hyponatremia
• 1.Hypovolemic hyponatremia
– Renal losses caused by diuretic excess, osmotic
diuresis, salt-wasting nephropathy, adrenal
insufficiency, proximal renal tubular acidosis,
metabolic alkalosis, and pseudohypoaldosteronism
result in a urine sodium concentration greater than 20
mEq/L
– Extrarenal losses caused by vomiting, diarrhea, sweat,
and third spacing result in a urine sodium concentration
less than 20 mEq/L
• Rx: Volume resuscitation with NS

Hyponatremia
• 2.Normovolemic hyponatremia
– When hyponatremia is caused by SIADH
(syndrome of inappropriate antidiuretic
hormone secretion), glucocorticoid deficiency,
hypothyroidism, or water intoxication, urine
sodium concentration is greater than 20 mEq/L
• Rx:
– Fluid restriction
– Correct endocrine abnormality

Hyponatremia
• 3.Hypervolemic hyponatremia
– If hyponatremia is caused by an edema-forming
state (eg, congestive heart failure, cirrhosis,
nephrotic syndrome), urine sodium
concentration is less than 20 mEq/L
– If hyponatremia is caused by acute or chronic
renal failure, urine sodium concentration is
greater than 40 mEq/L
• Rx: Correct underlying state

Causes of Hyponatremia Based
on Extracellular Fluid Volume
Status
• 1. Hypovolemic
• Gastrointestinal solute loss (diarrhea, emesis)
• Third-spacing (ileus, pancreatitis)
• Diuretic use
• Addison's disease
• Salt-wasting nephritis

Status
• 2. Euvolemic
• Syndrome of inappropriate antidiuretic hormone
(SIADH)
• Diuretic use
• Glucocorticoid deficiency
• Hypothyroidism
• Beer drinker's potomania,
• psychogenic polydipsia

Status
• 3. Hypervolemia with Decreased Effective
Circulating Blood Volume
• Decompensated heart failure
• Advanced liver cirrhosis
• Renal failure with or without nephrosis

93
Treatment of Hyponatremia
• Correct serum Na by 1mEq/L/hr
• Check serum Na q4hr
• Use 3% saline in severe hyponatremia
• Goal is serum Na 130
• Avoid too rapid correction:
– Central pontine myelinolysis
– Flash pulmonary edema

1.Depletion of sodium
• Sodium cannot be lost without water
• And isotonic or hypotonic loss would not be
expected to cause a fall in plasma sodium
concentration.

1.Depletion of sodium
• However, hyponatraemia can occur in sodium-
depleted patients, and is due either to
• Inappropriate replacement of fluid (e.g. containing
insufficient sodium) or,
• in severe sodium depletion, to the hypotonic
stimulus to vasopressin secretion, which overrides
the osmotic control and permits water retention at
the expense of a decrease in osmolality.

• It should be noted that, in patients with
hyponatraemia due to sodium depletion, clinical
signs of sodium depletion may be present.
• Unless the sodium loss is occurring through the
kidneys, increased aldosterone secretion should
cause maximal renal sodium retention and the
urinary sodium concentration will be low (usually
<20 mmol/L).

2.Water excess
• This gives rise to a dilutional hyponatraemia
with reduced plasma osmolality.
• It can occur acutely purely due to excessive water
intake, but this is rare.
• Normal kidneys are capable of excreting 1 L of
water per hour.

• Water intoxication and hyponatraemia will thus
be seen only
• when very large quantities of fluid are ingested
rapidly, as is seen in some patients with
psychoses.
• It can also occur in people who drink large
quantities of weak beer.

• The logical treatment of dilutional
hyponatraemia is;
• to restrict the patient's water intake to less than
that required to maintain normal water balance,
for example to 500-1000 mL/24 h.

• Water restriction is unpleasant and may be
impractical in chronic cases.
• Demeclocycline, a drug that antagonizes the
action of vasopressin on the renal collecting ducts,
has been used for this purpose.

• If patients are symptomatic, urgent correction of
the hyponatraemia is required.
• Hypertonic saline (3%) should be infused at a rate
sufficient to increase the plasma sodium
concentration initially by 1 mmol/L per hour but
not by >12 mmol/L over 24 h.
• Regular clinical assessment and measurement of
plasma sodium concentration are essential.

• In chronic dilutional hyponatraemia, correcting
the sodium concentration too rapidly risks causing
central pontine myelinolysis;
• a brain syndrome characterized by
• spastic quadriplegia,
• pseudobulbar palsy( it is a medical condition
characterised by the inability to control facial
movements (such as chewing and speaking)) and
• cognitive changes.

• Hypoxaemia or the presence of chronic liver
disease may increase this risk.
• This condition has a poor prognosis

3.Combined water and sodium
excess
• This is a frequent cause of hyponatraemia.
• It underlies the hyponatraemia of congestive
cardiac failure, hypoproteinaemic states and some
patients with liver failure.

• A decrease in the total negative charge on
plasma proteins, which contributes to the anion
gap, can reduce sodium in plasma.
• This is unusual, but it may contribute to
hyponatraemia in severe hypoalbuminaemia.

• The fact that there is sodium excess is indicated
by signs of increased ECF volume (e.g. peripheral
oedema).
• The logical treatment in these patients involves
measures to treat the underlying cause and remove
the excess sodium and water (e.g. with diuretics).
• Despite the hyponatraemia, saline should not be
given as these patients are already sodium
overloaded.

Electrolyte balance
• Na + (Sodium)
• Predominant extracellular cation
• 136 -145 mEq / L
• Pairs with Cl- , HCO3
- to neutralize charge
• Most important ion in water balance
• Important in nerve and muscle function
• Reabsorption in renal tubule regulated by:
• Aldosterone
• Renin/angiotensin
• Atrial Natriuretic Peptide (ANP)

Potassium K+
• 3.5-5.0 mEq/L
• Chief electrolyte of ICF
• Major mineral in all cellular fluids
• Aids in muscle contraction, nerve & electrical
impulse conduction, regulates enzyme activity,
regulates IC H20 content, assists in acid-base
balance
• Regulated by kidneys/ hormones
• Inversely proportional to Na

Potassium Homoeostasis
• Dietary potassium intake is of the order of 75-150
mmol/day, values higher in the range being
associated with a high intake of fruit and
vegetables.
• Extracellular potassium balance is controlled
primarily by the kidneys and, to a lesser extent, by
the gastrointestinal tract.
• In the kidneys, filtered potassium is almost
completely reabsorbed in the proximal tubules.

• Some active potassium secretion takes place in
the most distal part of the distal convoluted
tubules but potassium excretion is primarily a
passive process.
• The active reabsorption of sodium generates a
membrane potential that is neutralized by the
movement of potassium and hydrogen ions from
tubular cells into the lumen.

• Thus, urinary potassium excretion depends
upon several factors:
• the amount of sodium available for reabsorption
in the distal convoluted tubules and the collecting
ducts
• the relative availability of hydrogen and
potassium ions in the cells of the distal
convoluted tubules and the collecting ducts

• the capacity of these cells to secrete hydrogen
ions
• the circulating concentration of aldosterone
• the rate of flow of tubular fluid: a high flow rate
(e.g. osmotic diuresis, treatment with diuretics)
favours the transfer of potassium into the tubular
lumen.

• In the distal nephron, potassium is secreted in
exchange for either sodium or hydrogen ions:
increased delivery of sodium increases the
potential secretion of potassium.
• Aldosterone stimulates potassium excretion both;
• indirectly, by increasing the active reabsorption
of sodium in the distal convoluted tubules and the
collecting ducts, and
• directly, by increasing active potassium secretion
in the distal part of the distal convoluted tubules.

• Aldosterone secretion from the adrenal cortex is
stimulated indirectly by activation of the renin-
angiotensin system in response to hypovolaemia
and directly by hyperkalaemia.
• Since both hydrogen and potassium ions can
neutralize the membrane potential generated by
active sodium reabsorption, there is a close
relationship between potassium and hydrogen
ion homoeostasis.

• In an acidosis, hydrogen ions will tend to be
secreted in preference to potassium; in alkalosis,
fewer hydrogen ions will be available for
excretion and there will be an increase in
potassium excretion.
• Thus, there is a tendency to hyperkalaemia in
acidosis and to hypokalaemia in alkalosis.
• An exception to this tendency is renal tubular
acidosis caused by defective renal hydrogen ion
excretion.

• In this condition, because of the decrease in
hydrogen ion excretion, potassium secretion must
increase to balance sodium reabsorption.
• The result is the unusual combination of
hypokalaemia with acidosis.
• Healthy kidneys are less efficient at conserving
potassium than sodium: even on a potassium-free
intake, urinary excretion remains at 10-20
mmol/24 h.

• Since there is also an obligatory loss from the
skin and gut of approximately 15-20 mmol/24 h,
the kidneys cannot compensate if intake falls
much below 40 mmol/24 h.
• Potassium is secreted in gastric juice (5-10
mmol/L) and much of this, along with dietary
potassium, is reabsorbed in the small intestine.
• In the colon and rectum, potassium is secreted in
exchange for sodium, partly under the control of
aldosterone.

• Stools normally contain some potassium, but
considerable amounts can be lost in patients with
• fistulae or
• chronic diarrhoea (up to 30 mmol/L), or
• in patients who are losing gastric secretions
through persistent vomiting or
• nasogastric aspiration.
• Movement of potassium between the
intracellular and extracellular compartments
can have a profound effect on plasma potassium
concentration.

• The cellular uptake of potassium is stimulated by
insulin.
• Potassium ions move passively into cells from the
ECF in exchange for sodium, which is actively
excluded by a membrane-bound, energy-
dependent sodium pump.

• Hyperkalaemia can result if the activity of this
sodium pump is impaired or if there is damage to
cell membranes.
• Potassium uptake into cells is stimulated by
• insulin and β-adrenergic stimulation;
• α-adrenergic stimulation has the opposite effect.

• Transcellular shifts of hydrogen ions can cause
reciprocal shifts in potassium and vice versa.
• In a systemic acidosis;
• intracellular buffering of hydrogen ions results in
the displacement of potassium into the ECF.

• In alkalosis, there is a shift of hydrogen ions from
the ICF to the ECF, and a net movement of
potassium ions in the opposite direction, which
tends to produce hypokalaemia.
• Similarly, potassium depletion can lead to systemic
alkalosis.

Electrolyte balance
• K + (Potassium)
• Major intracellular cation
• 150- 160 mEq/ L
• Regulates resting membrane potential
• Regulates fluid, ion balance inside cell
• Regulation in kidney through:
• Aldosterone
• Insulin

Hypokalemia
• Serum level < 3.5mEq/L
• Results from decreased intake, loss via GI/Renal
& potassium depleting diuretics
• Life threatening-all body systems affected
• S/S muscle weakness & leg cramps, decreased GI
motility, cardiac arrhythmias
• Rx: diet/supplements/IV therapy

Lets think about …
Hypokalemia
a hypokalemia?
Renal Disease / CHF (dilutional)
Metabolic Alkalosis
Cushings Disease ( Na retention leads to K loss
• What are some conditions that might cause actual
loss of potassium from the body?
GI losses – nasogastric suctioning, vomiting,
diarrhea
Certain diuretic therapies
Inadequate intake – ( body cannot conserve K,
need PO intake)

• Cardiac arrest may occur when serum K levels
fall below 2.5 mEq/L. Why?
• Increased cardiac muscle irritability leads to
PACs and PVCs, then AF

Potassium Depletion and
Hypokalaemia
• Potassium depletion occurs when output exceeds
intake.
• Except in patients who are fasting, inadequate
intake is rarely the sole cause of potassium
depletion.

• However, increased loss of potassium, either
from the gut or (more often) through the kidneys,
is a frequent occurrence.
• If renal potassium excretion is <40 mmol/L in a
patient with hypokalaemia, excessive renal
excretion is unlikely to be the cause.
• Drug therapy is often implicated in the
pathogenesis of potassium depletion.

• When hypokalaemia is a result of potassium
depletion, it usually develops slowly and is only
corrected slowly when the cause is effectively
treated.
• In contrast, hypokalaemia as a result of
redistribution of potassium from the extra- to the
intracellular compartment usually develops
acutely, and can normalize rapidly.

Clinical features
• Even severe hypokalaemia may be asymptomatic.
Hypokalaemia causes hyperpolarization of
excitable membranes, thus decreasing their
excitability.
• When symptoms are present, they are related
primarily to disturbances of neuromuscular
function: muscular weakness, constipation and
paralytic ileus are common problems.

Management
• Although the plasma potassium concentration is a
poor guide to total body potassium, a plasma
concentration of 3.0 mmol/L generally implies a
deficit of the order of 300 mmol.
• The first step in the management of hypokalaemia
should be to identify and treat the causative
condition, but potassium replacement is frequently
required.

• Since any potassium deficit will be almost
entirely from the ICF but administered potassium
first enters the ECF, replacement must be
undertaken with care, particularly when the
intravenous route is used.
• As a guide, the following potassium dosages
should not be exceeded without good reason: a
rate of 20 mmol/h, a concentration of 40 mmol/L
in intravenous fluid or a total of 140 mmol/24 h.
• Thorough mixing with the bulk of the fluid to be
infused is vital.

Hyperkalemia
• Serum level >5 mEq/L
• Results from excessive intake, trauma, crush
injuries, burns, renal failure
• S/S muscle weakness, cardiac changes, N/V,
parathesias of face/fingers/tongue
• Rx:diet/meds/IV therapy/ possible dialysis.

Hyperkalemia
hyperkalemia?
Renal Disease=most common cause
Burns and other major tissue trauma
Metabolic Acidosis
Addison’s Disease ( Na loss leads to K retention )
• What are some conditions that might cause
potassium levels to rise in the body?
Certain diuretic therapies
Excessive intake – ( inappropriate supplements)

Hyperkalemia
• Cardiac arrest may occur when serum K levels rise
above 7mEq/L. Why?
• Decreased electrical impulse conduction leads to
bradycardia and eventually asystole.

Potassium Excess and
Hyperkalaemia
• Potassium excess can be due to excessive intake or
decreased excretion.
• A normal intake may be excessive if excretion is
decreased (e.g. in renal failure).
• Excessive intake is otherwise virtually always
iatrogenic (induced inadvertently by medical
treatment) and the result of parenteral
administration.

• Hyperkalaemia can result from potassium excess
but can also be a result of redistribution of
potassium from the intra- to the extracellular
compartment.
• This mechanism can sometimes give rise to
hyperkalaemia even in a patient who is potassium
depleted (e.g. in diabetic ketoacidosis).

• As with hypokalaemia, more than one cause of
hyperkalaemia may be present.
• Spurious hyperkalaemia, due to the leakage of
potassium from blood

Clinical features
• Hyperkalaemia is less common than hypokalaemia
but is more dangerous: through its effect on the
heart, it can kill without warning.
• It lowers the resting membrane potential, shortens
the cardiac action potential and increases the speed
of repolarization.
• Cardiac arrest in asystole or slow ventricular
fibrillation may be the first sign of hyperkalaemia.

• The risk increases significantly with potassium
concentrations;
• exceeding 6.5 mmol/L (particularly if the increase
has occurred rapidly);
• a true potassium concentration of >7.0 mmol/L is
a medical emergency.

• It is therefore necessary to be alert for this disorder
in appropriate circumstances,
• for instance in acute renal failure, to ensure that
effective early management is instituted.
• Characteristic ECG changes may precede cardiac
arrest.

Management
• Intravenous calcium gluconate (10 mL of a 10%
solution given over 1 min and repeated as
necessary) affords some degree of immediate
protection to the myocardium by antagonizing the
effect of hyperkalaemia on myocardial
excitability.
• Intravenous glucose and insulin, for example
500 mL of 20% dextrose with 20 units of soluble
insulin given over 30 min, promotes intracellular
potassium uptake.

• Salbutamol, which activates Na+,K+-ATPase, has
a similar effect.
• If insulin is used, blood glucose must be
monitored for the subsequent 6 h because of the
risk of hypoglycaemia.
• In an acidotic patient, hyperkalaemia can be
controlled temporarily by bicarbonate infusion
(using a 1.26% solution, not 8.4%, which risks
causing ECF volume expansion because of the
high sodium concentration).

• In acute renal failure and in other circumstances
where the hyperkalaemia is uncontrollable,
dialysis will be required.
• In chronic renal failure, restriction of potassium
intake and the administration of oral ion-
exchange resins are often successful in preventing
dangerous hyperkalaemia until such time as
dialysis becomes necessary for other reasons.

157
Calcium
• Normal 4.5-5.5 mEq/L
• 99% of Ca in bones, other 1% in ECF and soft
tissues
• Total Calcium – bound to protein – levels
influenced by nutritional state
• Ionized Calcium – used in physiologic activities –
crucial for neuromuscular activity

158
Calcium
• Required for blood coagulation, neuromuscular
contraction, enzymatic activity, and strength and
durability of bones and teeth
• Nerve cell membranes less excitable with enough
calcium
• Ca absorption and concentration influenced by Vit
D, calcitriol (active form of Vitamin D), PTH,
calcitonin, serum concentration of Ca and Phos

159
Causes of Hypocalcemia
• Most common – depressed function or surgical
removal of the parathyroid gland
• Hypomagnesemia
• Hyperphosphatemia
• Administration of large quantities of stored blood
(preserved with citrate)
• Renal insufficiency
• ↓ absorption of Vitamin D from intestines

160
Signs/Symptoms
• Abdominal and/or extremity cramping
• Tingling and numbness
• Positive Chvostek or Trousseau signs
• Tetany; hyperactive reflexes
• Irritability, reduced cognitive ability, seizures
• Prolonged QT on ECG, hypotension, decreased
myocardial contractility
• Abnormal clotting

161
Treatment
• High calcium diet or oral calcium salts (mild) - √
formulas for calcium content
• IV calcium as 10% calcium chloride or 10%
calcium gluconate – give with caution
• Close monitoring of serum Ca and digitalis levels
• ↓ Phosphorus levels ↑ Magnesium levels
• Vitamin D therapy

162
Hypercalcemia
• Causes
– Mobilization of Ca from bone
– Malignancy
– Hyperparathyroidism
– Immobilization – causes bone loss
– Thiazide diuretics
– Thyrotoxicosis
– Excessive ingestion of Ca or Vit D

163
Signs/Symptoms
• Anorexia, constipation
• Generalized muscle weakness, lethargy, loss of
muscle tone, ataxia
• Depression, fatigue, confusion, coma
• Dysrhythmias and heart block
• Deep bone pain and demineralization
• Polyuria & predisposes to renal calculi
• Pathologic bone fractures

164
Hypercalcemic Crisis
• Emergency – level of 8-9 mEq/L
• Intractable nausea, dehydration, stupor, coma,
azotemia, hypokalemia, hypomagnesemia,
hypernatremia
• High mortality rate from cardiac arrest

165
Treatment
• NS IV – match infusion rate to amount of UOP
• I&O hourly
• Loop diuretics
• Corticosteroids and Mithramycin in cancer clients
• Phosphorus and/or calcitonin
• Encourage fluids
• Keep urine acid

166
Evaluation
• Normal serum calcium levels
• Improvement of signs and symptoms

167
Magnesium
• Normal 1.5 to 2.5 mEq/L
• Ensures K and Na transport across cell membrane
• Important in CHO and protein metabolism
• Plays significant role in nerve cell conduction
• Important in transmitting CNS messages and
maintaining neuromuscular activity

168
Magnesium
• Causes vasodilatation
• Decreases peripheral vascular resistance
• Balance - closely related to K and Ca balance
• Intracellular compartment electrolyte
• Hypomagnesemia - < 1.5 mEq/L
• Hypermagnesemia - > 2.5 mEq/L

169
Hypomagnesemia
• Causes
– Decreased intake or decreased absorption or
excessive loss through urinary or bowel
elimination
– Acute pancreatitis, starvation, malabsorption
syndrome, chronic alcoholism, burns, prolonged
hyperalimentation without adequate Mg
– Hypoparathyroidism with hypocalcemia
– Diuretic therapy

170
Signs/Symptoms
• Tremors, tetany, ↑ reflexes, paresthesias of feet
and legs, convulsions
• Positive Babinski, Chvostek and Trousseau signs
• Personality changes with agitation, depression or
confusion, hallucinations
• ECG changes (PVC’S, V-tach and V-fib)

171
Treatment
• Mild
– Diet – Best sources are unprocessed cereal
grains, nuts, legumes, green leafy vegetables,
dairy products, dried fruits, meat, fish
– Magnesium salts
• More severe
– MgSO4 IM
– MgSO4 IV slowly

172
Treatment
• Monitor Mg q 12 hr
• Monitor VS, knee reflexes
• Precautions for seizures/confusion
• Check swallow reflex

173
Hypermagnesemia
• Most common cause is renal failure, especially if
taking large amounts of Mg-containing antacids
or cathartics; DKA with severe water loss
• Signs and symptoms
– Hypotension, drowsiness, absent DTRs,
respiratory depression, coma, cardiac arrest
– ECG – Bradycardia, CHB, cardiac arrest, tall T
waves

Treatment
• Withhold Mg-containing products
• Calcium chloride or gluconate IV for acute
symptoms
• IV hydration and diuretics
• Monitor VS, LOC
• Check patellar reflexes

Evaluation
• Serum magnesium levels WNL
• Improvement of symptoms

Phosphorous
• Normal 2.5-4.5 mg/dL
• Intracellular mineral
• Essential to tissue oxygenation, normal CNS
function and movement of glucose into cells,
assists in regulation of Ca and maintenance of
acid-base balance
• Influenced by parathyroid hormone and has
inverse relationship to Calcium

177
Hypophosphotemia
• Causes
– Malnutrition
– Hyperparathyroidism
– Certain renal tubular defects
– Metabolic acidosis (esp. DKA)
– Disorders causing hypercalcemia

Signs/Symptoms
• Impaired cardiac function
• Poor tissue oxygenation
• Muscle fatigue and weakness
• N/V, anorexia
• Disorientation, seizures, coma

179
Treatment
• Closely monitor and correct imbalances
– Adequate amounts of Phos
– Recommended dietary allowance for formula-
fed infants 300 mg Phos/day for 1st 6 mos. and
500 mg per day for latter ½ of first year
– 1:1 ratio Phos and Ca recommended dietary
allowance. Exception is infants, whose Ca
requirements is 400 mg/day for 1st 6 mos and
500 mg/day for next 6 months

Treatment
• Treatment of moderate to severe deficiency
– Oral or IV phosphate (do not exceed rate of 10
mEq/h)
– Identify clients at risk for disorder and monitor
– Prevent infections
– Monitor levels during treatment

Hyperphosphatemia
• Causes
– Chronic renal failure (most common)
– Hyperthyroidism, hypoparathyroidism
– Severe catabolic states
– Conditions causing hypocalcemia

182
Signs/Symptoms
• Muscle cramping and weakness
• ↑ HR
• Diarrhea, abdominal cramping, and nausea

Treatment
• Prevention is the goal
• Restrict phosphate-containing foods
• Administer phosphate-binding agents
• Diuretics
• Treat cause
• Treatment may need to focus on correcting
calcium levels

184
Evaluation
• Lab values within normal limits
• Improvement of symptoms

Fluids final 14.2.14

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Fluids final 14.2.14