Fluids

and
Electrolytes
A Thorough Guide covering Fluids,
Electrolytes and Acid-Base Balance of the
Human Body

David Andersson
© Copyright David Andersson 2018-All rights reserved.
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 TABLE OF CONTENTS

Introduction

Chapter I : Distribution of Body Fluids and Homeostasis

Chapter II : Fluid Volume Excess

Chapter III : Fluid Volume Deficit

Chapter IV : Acid-Base Homeostasis

Chapter V : Disorders of Acid-Base Balance: Acidosis and

Alkalosis

Chapter VI : Sodium – Homeostasis and Imbalances

Chapter VII : Chloride – Homeostasis and Imbalances

Chapter VIII : Potassium – Homeostasis and Imbalances

Chapter IX : Calcium – Homeostasis and Imbalances

Chapter X : Magnesium – Homeostasis and Imbalances

Chapter XI : Phosphorous – Homeostasis and Imbalances

Chapter XII : Imbalances in Common Medical Conditions

Conclusion

Answers to Exercises
 Introduction

Fluid maintenance remains one of the main foundations of medicine.

Fluids are deemed as being the most essential substance of life.
Around 60% of our body is made up of water, and this serves as a
medium for transport of both nutrients and waste products. The
electrolytes contained within the body water are responsible for the
body’s most basic functions, such as nerve function, and functioning
of voluntary and involuntary muscles, activating enzymes, and
release of hormones. Maintenance of these components in a
constant balance is essential, because the entire metabolic process
of the body depends on these components. Fluids and electrolytes
are not static, but interact continuously with each other, and with
other components of the body. It is essential to understand these
interactions, and the role they play in maintenance of health.
Imbalances in these substances within the body are responsible for
some of the most significant medical conditions and disorders. Any
patient, who has presented with a fairly serious medical illness, is
bound to have some kind of imbalance in the fluid-electrolyte levels.
All patients in intensive care units are routinely screened for such
imbalances. Thus, it is apparent that a medical professional needs to
have a firm grasped of the fundamentals of electrolytes, fluids and
acid-base balance in the body, so that effective treatment can be
carried out .

This subject is often confusing for both the beginner medical student
and the day to day medical practitioner. However, once the
underlying basic concepts of fluids and electrolytes are grasped, it
becomes easy to recognize imbalances in these systems, and it
follows that treatment becomes easier and more planned.
In this book, we will discuss the regulation of fluids, electrolytes, and
the acid-base system, and how these factors are interconnected.
When there is an imbalance in one of these electrolytes, the others
are usually affected. Similarly, electrolyte imbalances can arise from,
or be a result of, acid-base disorders. We will also discuss the signs
and symptoms of various imbalances, and touch upon the
management modalities for these imbalances. Common medical
conditions where there are massive imbalances are described in the
last chapter. There are summaries at the end of each chapter, that
help you quickly glance through essential information. Lastly, this
book tests what you have learned with post chapter tests.
 CHAPTER I : DISTRIBUTION OF BODY
FLUIDS AND HOMEOSTASIS
The concept of homeostasis
The term homeostasis is defined as the maintenance of nearly
constant conditions in the internal environment. This concept was
originally described by the French physiologist, Claud Bernard, who
stated that a free and independent existence was possible only
because of the stability of the internal milieu. It was Walter Canon in
1960 who coined the term ‘homeostasis’.
Most homeostatic mechanisms work by a negative feedback
mechanism. This mechanism consists of a sensor, which detects the
normal range of values, and an error detector, which detects if the
values become abnormal. This then sends a signal to the controller,
which interprets the abnormality and stimulates an effector, which
works to bring values back into the normal range.
This book discusses homeostasis of fluids, acid-base balance, and
electrolytes in the subsequent sections .
Body fluids in homeostasis

The human body is largely made up of water, which exists in the

form of several fluids. These fluids play an important role in day to
day functioning of the body. Fluids help in temperature regulation,
provide protection to vital organs, and lubrication to joint spaces.
They also act as a medium to dissolve solutes, and transport
essential compounds throughout the body. While water is the
solvent, body fluids contain several electrolytes, proteins, and cells,
which have to be maintained in homeostasis.
Distribution of body fluids

A large proportion of the human body is made up of fluids. Fluids

account for around 50% of total body weight in women and for
around 60% of total body weight in men. The proportion of fluids
decreases with age, and infants and children generally have a higher
percentage of fluid. Fluid proportion also decreases with increase in
body fat.

The fluids in the body are distributed between two compartments –

intracellular and extracellular. Intracellular fluids (ICF) account for
two-thirds of the total content, while extracellular fluids (ECF)
account for the remaining one third. The extracellular fluid
compartment is further divided into the intravascular and interstitial
compartments. The intravascular compartment is the fluid contained
in the blood vessels (plasma) and has one-fourth of the total ECF.
Interstitial fluid is the fluid that is present between the cells and forms
the remaining three-fourths of ECF.
The distribution of fluid between various body compartments is
outlined in Figure 1 .

Intracellular fluid:
The fluid inside the cell is referred to as cytosol. It contains various
enzymes, proteins, and ions. The intracellular fluid contains large
quantities of potassium and phosphate ions, and moderate quantities
of magnesium and sulfate ions. Sodium, chloride, and calcium ions
are present in low quantities. This is in contrast to the ions of the
extracellular fluid, which is discussed below.

Extracellular fluid:

The extracellular fluid consists of the interstitial fluid and plasma. The
interstitial fluid bathes and surrounds the cells of the body. They aid
in transport of nutrients to the cell and waste removal from the cell.
The plasma acts as a carrier for the various blood cells and proteins.
The ionic composition of the ISF and plasma is similar, however,
they differ in the protein composition. The ECF has large amounts of
sodium, chloride, and bicarbonate ions. The other ions, which are
high in the cytosol, are present only in small quantities here. The
plasma contains various dissolved proteins including albumins,
globulins, and fibrinogens. It also contains clotting factors and
glucose. The interstitial fluid is poorly permeable to proteins and
large molecules.

There is another fluid compartment, called the transcellular fluid

compartment, which forms 2.5% of the total body fluid content. This
does not form a separate fraction of the extracellular fluid, but is a
unique part of it. This fluid has protective and lubricative functions.
This is located in specific anatomical areas as follows:

Synovial fluid – Joints

Cerebrospinal fluid – Brain
Peritoneal fluid and pleural fluid – Chest cavity, around the
layers lining the heart and lungs respectively
Vitreous humor – Eyeballs

The values of important components of the body fluids are

summarized in Table 1.

TABLE 1 . CONCENTRATIONS OF ELECTROLYTES IN BODY

FLUIDS

COMPONENT INTERSTITIAL PLASMA INTRACELLULAR

FLUID (mOsm/L) FLUID (mOsm/L)
(mOsm/L)

Sodium 139 142 14

Chloride 108 108 4

Potassium 4 4.2 140

Calcium 1.2 1.3 0

 Bicarbonate 28.3 24 10

Phosphorous 2 2 11

Protein 0.2 1.2 4

Fluid movement between body compartments:

Both the intracellular fluid and extracellular fluid are bound by
membranes. These membranes act as a barrier to diffusion of fluids
from one compartment to another. While these membranes do not
easily allow the passage of solutes from one side of the membrane
to another, they allow the passage of water, they are hence referred
to as selectively permeable membranes. The process of diffusion of
water from a region of high water concentration to an area of low
water concentration is referred to as osmosis. The concentration of
water in any solution would depend on the amount of solutes that are
dissolved in that solution. The total number of solutes (electrolytes,
proteins, and other molecules) in a solution are measured in units
called ‘osmoles’, and their proportion in solution is expressed in
terms of ‘osmolality’. A fluid with greater osmolality is referred to as
hypertonic, and a fluid with lesser osmolality is referred to as
hypotonic. As plasma has higher quantity of proteins, it tends to have
higher osmolality as compared to interstitial fluid.

The interstitial fluid and plasma are separated by the walls of the
blood vessels. While the walls of the arteries and veins are thicker,
capillaries tend to have thin walls that allow easier movement of
water across them. The movement of water across capillaries is
governed by two forces – Hydrostatic pressure and Osmotic
pressure. Hydrostatic pressure is basically blood pressure, that is,
the pressure generated by contractions of the heart during systole. It
tends to drive fluid out of blood vessels. Osmotic pressure is the
pressure due to the hypertonicity of blood, which tends to retain fluid
within vessels.

At the arterial end of the capillary, hydrostatic pressure is always

greater. This causes fluid to move out of the blood vessels into the
interstitial compartment. At the venous end of the same capillary,
hydrostatic pressure decreases and the osmotic pressure is greater.
This causes most of the fluid to get reabsorbed into the capillary.
About 10% of the fluid fails to get reabsorbed, and this is directed
into the lymphatic system, which eventually returns it into circulation.
Factors that regulate fluid balance in the body :

The daily turnover of fluids in the body is around 2300 ml. A human
loses this amount of fluid every day. Fluid losses occur largely
through urine, and to a lesser extent through feces. Fluids are also
lost through evaporation from the skin surface, and through air
expelled from the lungs. This is an ongoing process, and is referred
to as insensible loss, as the patient is not aware of the loss.
Insensible skin loss is diffusion of water from the skin surface and
occurs independent of sweating. These fluids must be therefore
replenished daily. While most of the fluid input is from dietary
sources (food and water), a small amount is also produced from
metabolic pathways. This has been summarized in Table 2.

TABLE 2 . WATER TURNOVER IN THE HUMAN BODY

WATER INPUT WATER OUTPUT

Method Quantity (ml) Method Quantity (ml)

Ingested food
and Water 2000 Urine (variable) 1100
(variable)
 Metabolic 300 Feces 100
activity

Sweat 100

Insensible loss
(lungs and 700
skin)

Total 2300 ml Total 2300 ml

To maintain the fluid balance, a person needs to take in as much

water that leaves the body. If there is an imbalance between input
and output, various mechanisms in the body can correct it. The
proportion of fluid present in the body is reflected by the plasma
osmolality, which is basically the ratio of solutes to solvent. If the fluid
(solvent) proportion decreases, there is an increase in plasma
osmolality, and vice-versa. This change in osmolality is picked up by
osmoreceptors, which are located in the hypothalamus. The
hypothalamus then follows two pathways to correct this change:

Thirst mechanism: If the plasma osmolality increases, the

osmoreceptors stimulate the thirst center in the hypothalamus. This
triggers a subject to drink more water, thereby decreasing the
osmolality of plasma.

Antidiuretic hormone pathway: The hypothalamus controls the

release of a hormone called the anti-diuretic hormone (ADH) from
the posterior pituitary gland. The release of this hormone follows a
negative feedback loop. If the plasma osmolality is high, ADH
release is stimulated. ADH then acts on the kidneys, causing them to
reabsorb water from the distal convoluted tubules and collecting
duct. ADH acts on these systems by means of water channel
proteins, called aquaporins, which are moved from within the cell to
the cell surface. The cell thus becomes more permeable to water,
and increased quantities are absorbed. Since less water is excreted,
plasma osmolality decreases. On the other hand, if the plasma
osmolality decreases, release of ADH is suppressed, and more
water gets excreted via the kidneys. This causes the plasma
osmolality to rise again.

During increased plasma osmolality, ADH release also causes

peripheral arteriole constriction. This ensures that the blood flow is
directed towards the core of the body.

Factors that cause fluid imbalance

Certain factors can cause fluid imbalance in the body. Fluid
imbalance may be classified into three types as follows:

Hypovolemia: Decrease in the total body fluid is referred

to as hypovolemia. It may occur in the following
conditions:

Trauma: Due to blood loss

Dehydration: Excessive fluid loss, which can occur
in vomiting and diarrhea
Polyuria – excessive urination, which may be due to
drugs like diuretics
High fever – increases insensible losses

Hypervolemia: This is associated with fluid overload. It

may be iatrogenic, while treating hypovolemia, or may be
secondary to impaired excretion, as in kidney failure.
Normovolemia with fluid imbalance: This is seen
secondary to fluid resuscitation after major loss. In this
situation, fluid is retained within the intravascular
compartment. There is decreased tissue perfusion, which
may lead to multiorgan failure.

SUMMARY:
Fluids make up 50-60% of the body content, and are
essential for normal functioning of the body.
Fluids in the body are divided between two main
compartments – the intracellular and extracellular
compartments. The extracellular compartment consists of
interstitial fluid and plasma.
Fluids have a regular turnover in the body and move freely
between compartments.
Fluid balance is regulated and maintained by the
hypothalamus, and the antidiuretic hormone.
Fluid imbalance may occur in certain diseases and
conditions.
REFERENCES:

1. Guyton, A. C., & Hall, J. E. 1. (2006). Textbook of medical

physiology (11th ed.). Philadelphia : New Delhi: Elsevier
Saunders.

2. Cooper SJ. From Claude Bernard to Walter Cannon.

Emergence of the concept of homeostasis. Appetite 2008;
51: 419–427.

3. Modell H, Cliff W, Michael J, McFarland J, Wenderoth

MP, Wright A. A physiologist’s view of homeostasis.
Advances in Physiology Education. 2015;39(4):259-266.

4. Guyton, A. C., & Hall, J. E. (2000). The body fluid

compartments: extracellular and intracellular fluids;
interstitial fluid and edema. Textbook of medical
physiology, 11, 293.

5. Kreimeier U. Pathophysiology of fluid imbalance. Critical

Care. 2000;4(Suppl 2): S3-S7.
EXERCISES:

1. Which population subgroup has a higher percentage of

body fluid?

a. Adult female
b. Adult male
c. Infants
d. Obese people

2. Which of the following is not part of the extracellular

compartment?

a. Interstitial fluid
b. Synovial fluid
c. Cytosol
d. Plasma

3. Which of the following contributes to maximum excretion

of fluid from the body?

a. Sweat
b. Urine
c. Feces
d. Expiration

4. At the arterial end of a capillary, which of the following

statements is true?

a. Hydrostatic pressure > Osmotic pressure

b. Hydrostatic pressure = Osmotic pressure
c. Hydrostatic pressure < Osmotic pressure
d. None of the above

5. Which part of the body does insensible loss of fluid occur

from?

a. Kidney
b. Lungs
 c. Skin
d. Both b and c

6. On which area of the kidney does the antidiuretic

hormone effect its action?

a. Glomerulus
b. Proximal collecting tubule
c. Distal collecting tubule
d. Excretory duct

7. Which of the following is not an example of transcellular

fluid?

a. Cerebrospinal fluid
b. Pleural fluid
c. Renal tubular fluid
d. Synovial fluid

8. What is the amount of fluid produced by metabolic

processes in the body?

a. 300 ml
b. 500 ml
c. 700 ml
d. 900 ml

9. Which of the following ions is not found predominantly in

the intracellular region?

a. Potassium
b. Magnesium
c. Sodium
d. Phosphorous

10. Which of the following factors tends to excrete fluid from

the body?

a. Thirst mechanism
b. Increased ADH secretion
c. Decreased ADH secretion
d. None of the above
 CHAPTER II : FLUID VOLUME EXCESS
Fluid volume excess is also known as hypervolemia. This can occur
when the volume of fluid intake is far in excess of the fluid that can
be excreted from the body. The body has several mechanisms for
coping with increased fluid intake. It is only when these mechanisms
become saturated, which happens in advanced disease conditions
that the clinical manifestation of hypervolemia sets in.
Causes of hypervolemia:

There are two main reasons for which fluid content in the body would
increase:

Increased intake : Excessive intake rarely leads to hypervolemia as

the body automatically tends to excrete excess oral intake. However,
this can occur iatrogenically if excess fluid is given intravenously
during fluid resuscitation therapy.
Decreased output :

If the body fails to clear fluids at the same rate as intake, water
retention can occur, leading to hypervolemia. This can occur in two
ways:

Failure of excretion of total fluid :

This can occur if the kidney fails to function, and urine does
not form. The kidney retains water, which will later on move to
the interstitial space. This is also seen in mineralocorticoid
excess, which causes sodium and water retention by the
kidneys.

Failure of fluid movement between compartments:

In the previous chapter, movement of fluids between the

capillaries and interstitial spaces was discussed. If any
disease process disturbs this movement, fluids may
accumulate in the interstitial spaces. This can happen in the
following situations:

Decreased arteriolar resistance: This may be seen if

a patient is taking vasodilator drugs, or there is
insufficiency of the sympathetic nervous system.
This increases the hydrostatic pressure to drive
blood into the interstitial spaces.
Increased venous pressure: This may be seen in
cardiac failure, in venous obstruction, or in cases
where the valvular mechanism of the veins fails,
thereby causing backing up of blood from the veins
to the capillaries. The backed up blood volume
increases the hydrostatic pressure of the capillaries
and causes fluid shift into the interstitial space.
Decreased plasma osmotic pressure: This can
occur if the solutes of the plasma decrease. Plasma
protein loss can occur in nephritic syndrome and in
burn injuries. The production of plasma proteins
may be halted in conditions like liver cirrhosis, and
severe malnutrition. When the plasma osmotic
pressure is low, the capillaries fail to reabsorb the
interstitial fluid. This can cause fluid accumulation in
the interstitial space.
Increased capillary permeability: Inflammatory
reactions, immune reactions, ischemia, and
infections can cause capillaries to become ‘leaky’
which causes fluid escape from them to the
interstitial space.
Lymphatic blockage: A small percentage of
interstitial fluid is drained by lymphatics, and, if
these channels are blocked, fluid can accumulate
over time. This can occur in infectious conditions
such as filariasis, which cause lymph node swelling.
It can also occur when lymph nodes are surgically
removed after treatment for malignant disease.
The interstitial space has various coping mechanisms to deal with
the excess fluid overload. One mechanism is by increasing the
hydrostatic pressure of the interstitium, so that it resists the capillary
pressure and does not receive fluid. The second mechanism is by
increasing the lymphatic outflow. Lastly, in later stages, proteins get
washed out from interstitial spaces, reducing their osmotic pressure.
Fluid accumulation occurs only after these coping mechanisms
reach their limits. Therefore clinical manifestation of hypervolemia
generally is a sign of advanced disease.

Classification and clinical manifestations of hypervolemia:

When there is fluid volume excess, the water accumulates in tissues
just beneath the skin. This type of condition is referred to as edema.
Edema usually occurs in dependent areas of the body. The edema
may be of two types – pitting or non-pitting. In pitting edema, if
pressure is applied to the edematous area, the indentation persists
even after pressure is removed. This usually occurs when the
interstitial space had fluid but low concentration of protein. In non-
pitting edema, the indentation does not persist.

The location of edema may give a clue as to the underlying cause of

fluid retention. Based on the location, the various types of edema are
as follows :
Generalized edema:

The edema occurs in multiple organs as well as the periphery. This

is often seen in cardiac failure, nephrotic syndrome, and severe
nutritional deficit. Ascites is a special type of edema that occurs in
liver cirrhosis, and involves accumulation of fluid in the peritoneal
cavity. Severe generalized edema is referred to as anasarca.

Organ specific edema:

In pathology or inflammation of specific organs, water retention will
occur in that organ alone. A few examples are detailed in the table
below:
 TABLE 1 . EXAMPLES OF ORGAN SPECIFIC EDEMA

Organs affected Conditions in which this is

likely to occur

Cerebral edema – brain Lack of oxygenation to brain.

Pulmonary edema – lungs Left ventricular failure,

inhalation of toxic agents

Cutaneous edema – skin Inflammatory reactions e.g.

insect bites, myxedema

Periorbital edema Trauma to the orbit

Lymphedema Areas where lymph drainage is

blocked e.g. elephantiasis of the
foot in filariasis.

The clinical features of water retention will also depend on the area
where edema occurs. Most cases of edema present with swelling of
the involved region. Since the skin over the area is stretched, there
may also be pain in that region. Limitation of motion of the affected
limb may also occur. Organ specific edema will have symptoms
related to that organ.

Peripheral edema presents with swelling of the ankles and

wrists.
Pulmonary edema presents with shortness of breath.
Cerebral edema presents with drowsiness, or loss of
consciousness.
Effusions: In organ specific edema, fluid can go into
potential spaces such as pleura or pericardium. Pleural
 effusion presents with shortness of breath, and pericardial
effusion has breathlessness in addition to muffled heart
sounds.

Diagnostic tests:
If a patient presents with unexplained edema, a series of tests may
be performed to diagnose or rule out systemic diseases. These
include the following:

Brain natriuretic peptide measurement: for congestive

cardiac failure
Blood urea nitrogen, creatinine, and urine analysis : for
renal disease
Liver enzymes and albumin measurement: for liver
disease
Ultrasonography, D-dimer tests: when deep vein
thrombosis and venous insufficiency of lower limbs is
suspected.

Management of hypervolemia:

The underlying cause of hypervolemia must be identified and

managed appropriately. Once the disease process comes down,
edema tends to resolve. Certain measures, however, can be taken to
help reduce the amount of water retention. These are as follows:

Proper positioning: Elevating swollen legs causes fluid to

drain from them as it works against gravity.
Intermittent pneumatic compression devices: These
devices provide external pressure that forces blood and
lymph out of that area.
Limiting sodium intake in diet may help reduce water
retention.
Diuretics: these are drugs that promote excretion of water
from the kidneys. They help reduce the overall water
content in the body. They are useful in cardiac and liver
 disease, but must not be used in conditions of increased
capillary permeability.

SUMMARY:

Fluid retention or hypervolemia occurs if there is

increased intake or decreased output.
Decreased output is more common and occurs when the
kidneys fail, or interstitial fluid fails to move into capillaries.
The main clinical manifestation of hypervolemia is edema.
It may be generalized or localized, pitting or non-pitting.
Edema presents with swelling, pain, limitation of motion,
and organ specific features.
Resolving the underlying cause can remove edema. Other
measures include positioning, pressure devices, and
diuretic drugs.
REFERENCES:

1. Braunwald E, Loscalzo J. Edema. In: Longo DL, Fauci AS,

Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds.
Harrison’s Principles of Internal Medicine. 2011 18th ed.
New York, NY: McGraw-Hill

2. Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema:

diagnosis and management. Am Fam Physician. 2013 Jul
15;88(2).

3. O’Brien JG, Chennubhotla SA, Chennubhotla RV.

Treatment of edema. Am Fam Physician.
2005;71(11):2111-2117

4. Rockson SG. Lymphedema. Am J Med. 2001;110(4):288-

295
EXERCISES:

1. Which one of these options causes water retention?

a. Heart attack
b. High blood pressure
c. Kidney Failure
d. All the above

2. Which of these mechanisms does not cause water

retention?

a. Increased plasma osmotic pressure

b. Reduced plasma osmotic pressure
c. Increased capillary permeability
d. Increased tissue osmotic pressure

3. What electrolyte contributes to increased water retention?

a. Potassium
b. Magnesium
c. Sodium
d. Calcium

4. Which of the following is not a symptom of edema?

a. Swelling
b. Pain
c. Dizziness
d. Limitation of motion

5. Ascites is a type of edema that occurs in which one of the

following conditions?

a. Renal failure
 b. Liver failure
c. Cardiac failure
d. Pulmonary failure

6. Which of the following is not a coping mechanism that the

interstitial fluid follows in fluid overload?

a. Increasing the hydrostatic pressure of the

interstitium
b. Increasing the lymphatic outflow
c. Decreasing the osmotic pressure of the interstitium
d. Increasing the hydrostatic pressure of the plasma

7. Elephantiasis is a type of edema that is seen in which type

of infection?

a. Malaria
b. Dengue
c. Filariasis
d. Amoebiasis

8. What is the term used to refer to generalized edema?

a. Amyloidosis
b. Anasarca
c. Lymphedema
d. None of the above
 9. Pericardial effusion is characterized by which of the
following clinical features?

a. Increase heart sounds

b. Muffled heart sounds
c. Irregular heart sounds
d. All of the above

10. In which of the following causes of fluid overload are

diuretics contraindicated?

a. Renal failure
b. Increased capillary permeability
c. Heart failure
d. None of the above
 CHAPTER III : FLUID VOLUME DEFICIT
A fluid volume deficit can happen if the person loses more fluids from
his body than he takes in. Fluid loss can occur from any of the
compartments. Fluid loss that occurs exclusively from the
intravascular space is referred to as hypovolemia. On the other
hand, dehydration is a form of fluid deficit that is spread across all
the fluid compartments.

DEHYDRATION:
This is a deficit of total body water. There is loss of fluid from all the
body compartments.
Causes:
Dehydration can occur in two scenarios – if the total water intake has
decreased, or if there is excessive total water loss from the body.

Decreased intake:

Blunted thirst mechanism – seen in elderly patients

Lack of available water – This can occur in extreme
situations, such as when a person is lost in the
desert, or at sea.
When a patient is asked to be ‘nil per mouth’ before
surgery, and adequate fluids are not given
intravenously.

Excessive water loss:

Vomiting and diarrhea can quickly cause loss of

large volumes of water.
Excessive sweating: can occur with sports,
overexertion, and in high fevers.
Excessive urination: In uncontrolled diabetics, and
with drugs such as diuretics.
Classification of dehydration:
Generally, when body fluid is lost, there is variable loss of
electrolytes as well, particularly sodium. Depending on the amount of
electrolyte that is lost, dehydration can be classified as follows:

TABLE 1 . TYPES OF DEHYDRATION

Type of dehydration Plasma osmolarity Condition seen

Isonatremic 130 – 150 mEq/L Equal loss of

sodium and water

Hyponatremic < 130 mEq/L Lost fluid has

excessive sodium

Hypernatremic > 150 mEq/L Lost fluid has

minimal sodium

Signs and symptoms:

The signs and symptoms depend on the stage of dehydration in
which the patient presents .

Mild dehydration (fluid loss of 30-50 ml/kg)

The earliest symptom is a feeling of dryness of mouth and

tongue.
Headache, tiredness, and loss of appetite
Reduced urination (unless the cause is polyuria). This is a
sign that can be checked in infants, who will have fewer
wet diapers.
Infants and children will also present with irritability
Capillary refill time is 2 seconds
 Heart rate is normal or increased. Blood pressure and
respiratory rate are normal.

Moderate dehydration: (fluid loss of 60-100 ml/kg)

Dryness of mouth and mucous membranes increases

Sunken face and eyes
Skin is dry and inelastic, turgor is slow
There will be reduced lacrimation, along with decreased
urine output.
Dizziness and lethargy may be present.
Capillary refill time: 2-4 seconds
Heart rate increases, blood pressure drops and
respiratory rate increases.

Severe dehydration: (fluid loss of 90-150 ml/kg)

The features resemble that of moderate dehydration, but

are increased in severity.
Patient will be disoriented and confused.
Skin and mucous membranes become parched and
cracked. Skin turgor is lost completely and tenting takes
place.
Capillary refill time is more than 4 seconds.
Urinary output is very low; anuria may be presen t

Consequences of severe dehydration:

Seizures: This can occur if the plasma sodium falls.

Pontine necrosis and cerebral edema: This is a consequence of

rapid rehydration, and not the dehydration process itself. Rapid
rehydration causes rapid rush of water into cells, which may rupture,
leading to cerebral edema.
Management of dehydration:

Mild dehydration: This can be corrected by rehydrating the patient

with water alone. The patient can take sips of water, or ice chips to
correct this state.

Moderate dehydration: Usually this involves loss of water as well as

electrolytes. Oral rehydration solution (ORS) is indicated for
replacement of water as well as lost electrolytes such as sodium and
potassium. It is particularly useful in malnourished children from
developing countries, who are affected with diarrhea. If oral intake is
ineffective because of repeated vomiting, replacement can be done
via nasogastric tube.
Severe dehydration: This requires prompt replacement of fluids, but
at a slow rate to avoid the complications mentioned above.
Intravenous or intraosseous lines must be established. Fluid
replacement is preferably done with isotonic solutions such as
Ringer’s lactate or 0.9% sodium chloride. If there is symptomatic
hyponatremia, replacement is done with slow infusion of 3% saline
solution. Repeated monitoring is essential to adjust the amount of
fluid given.

Supportive therapy and treating the cause of dehydration are

important steps in management. Anti-emetics such as Ondansetron
have been found effective in severe vomiting. However, routine use
of antibiotic therapy and anti-diarrheal agents is not recommended .

HYPOVOLEMIA:

In hypovolemia, fluid is lost from the intravascular compartment

alone. It is also called volume depletion. This can occur when whole
blood is lost (e.g. during trauma or surgery), or when plasma alone is
lost (e.g. in burn injuries). It can also occur as a consequence of
dehydration, when excessive sodium is lost from the body.

The most important consequence of hypovolemia is that the body

goes into a shock response in order to sustain life and function. This
is called hypovolemic shock. Since loss of whole blood is the
commonest cause, it is also referred to as hemorrhagic shock.
Causes:
 External blood/plasma loss: Traumatic injuries, burns
Internal blood loss: internal organ injury, rupture of
aneurysms, bleeding gastrointestinal ulcers.
Pregnancy related disorders : ectopic pregnancy, placenta
previa, placenta abruption
Extreme fluid loss in diarrhea, vomiting etc.

Signs and symptoms:

The clinical presentation of shock depends on the severity, which in
turn depends on the volume of blood that is lost.

Class I:

Less than 15% of blood volume is lost

No symptoms
Blood pressure, pulse rate, and respiratory rate are
normal. Mild tachycardia may be seen.
Capillary refill time is about 3 seconds.

Class II:

Blood volume loss is 15 – 30%

Clinically manifested by pallor and anxiety
Tachycardia and tachypnoea is seen. Blood pressure may
be increased slightly.

Class III:

Blood volume loss is 30 – 40%

Mental status is altered; confusion and agitation may be
seen.
Oliguria is seen
Marked tachycardia and tachypnoea is present. Systolic
blood pressure begins to fall.

Class IV:

Blood volume loss is more than 40%.

 Depression of mental status and loss of consciousness.
Skin is pale and cold.
Minimal or no urination.
Extreme fall in systolic blood pressure; tachycardia is
seen.

Management of hypovolemic shock:

Hypovolemic shock is a life threatening condition and therefore must
be managed promptly both in the field and in the emergency
department. There are three basic goals of management:

Maximizing oxygen delivery to the tissues:

Airway must be cleared of obstruction

Oxygen must be delivered at high flow to improve
the concentration of oxygen being delivered.

Fluid resuscitation:

Two wide bore intravenous lines must be started for

fluid resuscitation. Intraosseous lines can be used in
children and intra-arterial lines may be used in
severe cases.
Initially, fluid bolus is given with crystalloids. A bolus
of 1 – 2 liters is given in adults and 20 ml/kg is given
for children. Colloid solutions are not preferred for
initial resuscitation.
Further fluids are given based on response
assessment; in the meantime, patient’s blood is sent
for typing and cross-matching in case further blood
transfusions are required.
If there is no response to the fluid bolus, or if the
patient presents with Class IV shock, type O-
negative blood must be given.

Controlling ongoing blood losses:

 Ongoing blood losses must be controlled after
obtaining intravenous access. Direct pressure must
be applied on areas of active bleeding in the field;
bleeding vessels can be identified and ligated in the
emergency room.
Fractures of long bones must be reduced and
splinted.
Bleeding from nose and other cavities must be
controlled by packing.
Surgical intervention may be needed for bleeding
control; e.g. removal of spleen.

SUMMARY:

Fluid deficit may include either fluid loss from all the body
compartments (dehydration), or loss from only the
intravascular compartment.
Dehydration occurs either due to decreased intake of
water or excessive loss of fluids from the body.
It presents with dryness of skin and mucous membranes,
headache, and lethargy. Later stages may show mental
confusion and seizures.
Dehydration must be treated with oral rehydration
solutions or intravenous fluid therapy.
Hypovolemia is life threatening and can cause shock.
It is manifested as tachycardia, reduced blood pressure,
and mental depression or loss of consciousness.
The goals in management of hypovolemia include
maximizing oxygen delivery to tissues, prompt fluid
resuscitation and replacement, and preventing further
loss.
REFERENCES:

1. Dill DB, Costill DL. Calculation of percentage changes in

volumes of blood, plasma, and red cells in dehydration.
Journal of applied physiology. 1974 Aug;37(2):247-8.

2. Dalal KS, Rajwade D, Suchak R. “Nil per oral after

midnight”: Is it necessary for clear fluids? Indian Journal
of Anaesthesia. 2010;54(5):445-447. doi:10.4103/0019-
5049.71044.

3. Colletti JE, Brown KM, Sharieff GQ, Barata IA, Ishimine

P, ACEP Pediatric Emergency Medicine Committee. The
management of children with gastroenteritis and
dehydration in the emergency department. J Emerg Med.
2010 Jun. 38(5):686-98

4. Goldman RD, Friedman JN, Parkin PC. Validation of the

clinical dehydration scale for children with acute
gastroenteritis. Pediatrics. 2008 Sep. 122(3):545-9

5. Gulati A. Vascular endothelium and hypovolemic shock.

Curr Vasc Pharmacol. 2016. 14(2):187-95

6. Reinhart K, Perner A, Sprung CL, et al. Consensus

statement of the ESICM task force on colloid volume
therapy in critically ill patients. Intensive Care Med. 2012
Mar. 38(3):368-83
EXERCISES:

1. Which is the earliest manifestation of dehydration?

a. Lethargy
b. Confusion
c. Dry mouth
d. Seizures

2. What is the commonest cause of dehydration in children

in developing countries?

a. Insufficient intake
b. Fluid shift
c. Diarrhea
d. Polyuria

3. What is the ideal treatment for moderate dehydration due

to diarrhea in children?

a. Plain Water
b. Oral rehydration solution
c. Intravenous fluids
d. Glucose drinks

4. Hypovolemia is a deficit of fluid in which compartment?

a. Extra cellular Fluid

b. Intra cellular fluid
c. Interstitial Fluid compartment
d. Intravascular compartment

5. Which of the following is not an immediate goal for

managing hypovolemia?

a. Maximizing oxygenation
b. Reducing neurological deficit
c. Controlling ongoing blood loss
d. Fluid replacement
 6. Mild hypovolemia involves loss of how much quantity of
fluid?

a. less than 5%
b. Less than 10%
c. Less than 15%
d. Less than 20%

7. What is the possible consequence of rapid intravenous

rehydration?

a. Cerebral edema
b. Pulmonary edema
c. Cardiac ededma
d. Generalized edema

8. What is the clinical presentation of vitals seen in

hypovolemic shock?

a. Decreased pulse and blood pressure

b. Increased pulse and blood pressure
c. Decreased pulse, increased blood pressure
d. Increased pulse, decreased blood pressure.

9. In which stage of shock does the mental status alter?

a. Stage I
b. Stage II
c. Stage III
d. Stage IV

10. What is the initial fluid preferred for resuscitation in

hypovolemic shock?

a. Crystalloids
b. Colloids
c. Whole blood
d. Packed cells
 CHAPTER IV : ACID–BASE HOMEOSTASIS
While the volume of fluids in the body must be maintained in perfect
balance, its composition and properties, such as pH, must also be
maintained in harmony. The homeostasis of individual electrolytes
will be discussed in future chapters. In this chapter, the regulation of
pH, or maintenance of the body’s acid-base balance is discussed in
detail.
The body maintains the pH if the intracellular fluids and extracelluar
fluids remain at a constant level. ECF is slightly basic, and ranges
from 7.35 to 7.45, usually it is maintained optimally at 7.40. This
optimum pH provides an ideal environment for components of the
fluid to function. The immune system can function only at this optimal
pH, and above or below this pH, there is a tendency for proteins to
get denatured, leading to loss of function.

There are three main methods by which the body regulates acid-
base homeostasis:

Chemical buffering mechanisms

Renal regulation of pH
Respiratory regulation of p H

Chemical buffering systems:

Chemical buffers are compounds that bring back the pH of body
fluids to their normal value, thereby helping to maintain homeostasis.
They are the first line of defense against sudden changes in pH.
These buffers are basically molecules or compounds that are
capable of combining with hydrogen ions, or releasing them as per
the need. There are three important chemical buffers present in the
human body:

Bicarbonate buffer:
 The bicarbonate buffer is the most important chemical
buffer system and is largely responsible for maintaining
the pH of the extracellular fluid.

Bicarbonate ion (HCO3-) can combine with hydrogen ion

(H+) to form carbonic acid (H2CO3). This can be
represented by the equation below:
HCO3- + H+ -- H2CO3

When the pH of the ECF falls, it contains excess H+ ions,

which combine with HCO3. Therefore the above equation
shifts to the right. The carbonic acid further dissociates
into carbon dioxide and water (CO2 and H2o), and excess
carbon dioxide is removed by the lungs.

When the pH of the ECF rises, there is a deficit of H+

ions. So carbonic acid dissociates, and the above
equation shifts to the left.
At normal pH, the usual ratio of bicarbonate to carbonic
acid is 20:1.

The bicarbonate buffer system depends on two factors:

Firstly, normal levels of bicarbonate must be present in the
body. Secondly, the respiratory system must function
properly. If it does not, carbon dioxide levels may be
abnormal which would affect the efficacy of this system.
The bicarbonate system and respiratory regulation are
interlinked, as the carbon dioxide produced affects
respiratory regulation. This can be seen in the next
section.

Protein buffer:

This buffer mechanism acts both intracellularly and

extracellularly.
 Proteins are made up of amino acids. Each amino acid
contains a carboxyl group (COO-) and an amino group
(NH2+).

Both the carboxyl and amino groups are capable of

adding on another hydrogen ion when needed, and can
transform into COOH and NH3+ under acidic conditions.
These hydrogen ions can be released from the amino
acids when the pH increases.

Phosphate buffer:

Phosphate plays an important role in buffering of

intracellular fluid.

Phosphate ions (HPO4-) can take up excess hydrogen

ions, under conditions of acidity, to become dihydrogen
phosphate (H2PO4) or trihydrogen phosphate (H3PO4).
They release these ions when the pH increases.

Respiratory regulation of pH :

The rate of respiration is one of the mechanisms of maintaining acid-

base balance in the body.
In general, the pH of the blood, and content of carbon dioxide
(pCO2) in the blood and extracellular fluid, can be sensed by central
chemoreceptors. These chemoreceptors are located in the medulla
oblongata of the brain .

If there is any change in the pH or pCO2, this is picked up by the

chemoreceptors, which then send signals to the respiratory center,
located in the pons and medulla oblongata.

The respiratory center sends efferent signals via motor neurons to

the respiratory muscle, namely the diaphragm and intercostal
muscles. This will alter the rate of contraction of these muscles,
which in turn will alter the rate of ventilation.

Normally, the pCO2 (partial pressure of carbon dioxide) is 40 mmHg,

and alveolar ventilation allows about 15 mol of CO2 to be excreted
each day.
If the acidity of blood rises (low pH), the pCO2 increases. This
causes increase in alveolar ventilation, which will blow off more
carbon dioxide, thereby decreasing the pCO2 level.

On the other hand, if the blood becomes more alkaline (high pH), the
pCO2 falls. This causes the alveolar ventilation to decrease, which
retains CO2 in the blood, and allowing the pCO2 to rise.

It must be remembered, from the previous section, that CO2 in the

blood is a product of carbonic acid breakdown, and is formed in
response to low pH. Therefore high pCO2 reflects low pH and vice
versa.

Renal regulation of pH:

The kidneys play an extremely important role in acid-base balance,

because, they are capable of taking up the slack if the other systems
stop functioning for any reason. There are two ways in which the
kidneys regulate acid-base balance:

Reabsorption of bicarbonate into the body

Excretion of acids into the urine .

Reabsorption of bicarbonate:

Almost all the bicarbonate present in the plasma is filtered

by the glomerulus, which is roughly 4000 to 5000
mmol/day.

However, this is later reabsorbed. 85 – 90% of the

bicarbonate is reabsorbed in the proximal tubule, while the
 rest gets reabsorbed in the intercalated cells of the distal
convoluted tubule and collecting duct.

Within the tubular cell, water and carbon dioxide, in the

presence of the enzyme carbonic anhydrase, combine to
form bicarbonate and hydrogen ions:
H2O + CO2 - H+ + HCO3-

The hydrogen ion leaves the tubular cell and enters the
lumen, using Na+H+ antiporter, which exchanges H+ for
Na+.

Within the lumen, the hydrogen ion combines with the

filtered bicarbonate ion, once again forming carbon
dioxide and water.
Carbon dioxide, which is lipid soluble, enters the cell
again, and combines with water to produce bicarbonate
and hydrogen ion. Thus, while bicarbonate is reabsorbed,
hydrogen ion is not lost; instead, there is a net gain of one
sodium ion.

Excretion of acids:

There are two types of acids which are excreted

Ammonium (NH4+): Ammonia (NH3) is produced as a breakdown
product of glutamine, which is present in the tubular filtrate, as well
as the peritubular capillaries. This tends to combine with hydrogen
ions and is excreted in the collecting duct as ammonium. This serves
to reduce the pH of the final urine as well.

Titrable acids: Titrable acids include phosphates, citrates, and

sulfates. These compounds have the capacity to combine with
hydrogen ions and get excreted from the kidney, thereby reducing
the overall pH.

SUMMARY:
For optimum functioning of the body, the pH of
extracellular fluid has to be maintained at 7.35 to 7.45.

This is done by three mechanisms – chemical buffering

systems, respiratory mechanisms, and renal mechanisms.
Chemical buffers include bicarbonates, phosphates, and
protein buffers. These compounds are capable of binding
with or dissociating from hydrogen ions as the need
arises.

Respiratory system regulates pH by controlling the

amount of carbon dioxide that is exhaled. In acidic states,
excess CO2 is exhaled, and in basic states, CO2 is
retained to maintain the pH.

Renal system regulates pH by two methods- firstly, by

absorbing bicarbonate back from the renal tubular fluid,
and secondly, by excretion of ammonium and other acids,
that removes excess hydrogen ions from the body.
REFERENCES:

1. Hamm, L. L., Nakhoul, N., & Hering-Smith, K. S. (2015).

Acid-Base Homeostasis. Clinical Journal of the American
Society of Nephrology : CJASN, 10(12), 2232–2242.

2. Boyd, D. (1974). Acid base homeostasis and its disorders.

Chest, 66(2), p.25.

3. Hood VL, Tannen RL. (1998). Protection of acid-base

balance by pH regulation of acid production. N Engl J
Med 339: 819–826.

4. Tannen RL. (1983). Ammonia and acid-base homeostasis.

Med Clin North Am; 67(4): 781-98.
EXERCISES:

1. What is the optimum pH of human blood?

a. 7.20
b. 7.30
c. 7.40
d. 7.50

2. Which of the following is not a component of the chemical

buffering system?

a. Ammonium
b. Bicarbonate
c. Protein
d. Phosphate

3. What is the normal ratio of bicarbonate to carbonic acid in

the body?

a. 10:1
b. 30:1
c. 20:1
d. 40:1

4. The efficacy of the bicarbonate buffer depends on proper

functioning of which of the following systems?

a. Renal system
b. Cardiac system
 c. Nervous system
d. Respiratory system

5. Which component of the amino acid acts as a chemical

buffer?

a. R group
b. Central carbon atom
c. Carboxyl group
d. Hydrogen atom

6. Which of the following buffers has a predominantly

intracellular effect?

a. Ammonium
b. Phosphate
c. Bicarbonate
d. Proteins

7. In which part of the body are the chemoreceptors for

PaCO2 located?

a. Lungs
b. Carotid body
c. Pons
d. Medulla oblongata

8. How much carbon dioxide is excreted by the lungs per day

under normal conditions?
 a. 5 mol
b. 10 mol
c. 15 mol
d. 20mol

9. In which area of the kidney does most of the bicarbonate

reabsorption occur?

a. Proximal convoluted tubule

b. Descending lop of Henle
c. Thick ascending loop of Henle
d. Distal convoluted tubule

10. Which amino acid predominantly contributes to the

production of ammonium ion?

a. Aspartate
b. Glutamine
c. Methionine
d. Arginine
 CHAPTER V : DISORDERS OF ACID-BASE
BALANCE - ACIDOSIS AND ALKALOSIS
The normal pH of blood is 7.35 to 7.45. If the pH moves beyond
these limits, acid-base disorders can result. Acidosis occurs when
arterial blood pH moves below 7.35, whereas alkalosis occurs when
the pH rises above 7.45.
Depending on the mechanism of homeostasis that is disturbed or
overloaded, acid-base disorders may be categorized as respiratory
disorders or metabolic disorders. Metabolic disorders are primarily
due to changes in levels of bicarbonate within the body, while
respiratory disorders are due to changes in the partial pressure of
carbon dioxide.

Having either a metabolic or a respiratory acid-base disorder is

referred to as a ‘simple’ disorder. There is another category of acid-
base disorders, namely the mixed disorders, which have both
metabolic and respiratory components. This may be because the
body is trying to compensate for one type of disorder. However, it
usually occurs independently. Here both metabolic and respiratory
disorders can co-exist because of independent pathological
processes in the disease. Such conditions can lead to extreme
changes in pH and are dangerous.

TESTS FOR DIAGNOSIS OF ACID-BASE DISORDERS:

In order to correctly diagnose the type of acid-base disorder, certain
tests must be carried out in a step-wise manner. These are
described as follows:

Arterial blood gases:

Blood drawn from the arteries is analyzed for pH and

PaCO2. From these values, the bicarbonate is calculated
using the following equation:
 pH = 6.1 + log HCO3-

PaCO2 x 0.0301

An increase in pH indicates alkalosis, while a decrease in

pH indicates acidosis.
Respiratory acidosis and alkalosis would be associated
with increase and decrease in PaCO2 respectively.
Bicarbonates are normal.
Metabolic acidosis and alkalosis would be associated with
a respective decrease and increase in HCO3.
However, in compensation, the above values may be
altered.

TYPE OF pH pCO2 HCO3- Compensatory

ACID mechanism
BASE
DISORDE
R

Metabolic Decrease Normal Decrease Respiratory-

acidosis d d reduced pCO2

Metabolic Increased Normal Increased Respiratory-

alkalosis increased
pCO2

Respirator Decrease Increased Normal Renal –

y acidosis d increased
HCO3-

Respirator Increased Decrease Normal Renal –

y alkalosis d decreased
HCO3 -
Anion gap:

Anion gap is defined as the difference between the

cations and anions in the blood plasma. It is therefore a
measure of the neutrality of plasma.
The major cation in the blood is sodium, and the major
anions in blood are chloride and bicarbonate.
The anion gap is measured as: Na - (Cl + HCO3).
The normal anion gap is 6 – 12 mEq/L.
This gap may increase in there is a decrease in
unmeasured anions, and, rarely, due to increase in
unmeasured cations. The anion gap is useful in
diagnosing type of metabolic acidosis.

METABOLIC ACIDOSIS
This is a condition where there is a relative decrease in serum
bicarbonate concentration.

Causes:
The cause can be of two types depending on the anion gap
measurement.

Normal anion gap:

In these cases, the anion gap is normal, usually because there is an
increase in chloride, which has compensated for the decrease in
bicarbonate. Hence this variety is also referred to as hyperchloremic
acidosis. This may be due to:

Gastric losses – vomiting, diarrhoea

Acidifying drugs – Calcium chloride
Renal tubular acidosis
Hyperkalemia – due to drugs, or renal dysfunctio n

High anion gap:

The anion gap is increased due to reduction in bicarbonate, or
increase in acidifyting cations. These are seen in the following
conditions:

Diabetic ketoacidosis
Ketoacidosis due to alcoholism and starvation
Lactic acid acidosis
Renal failure
Toxins such as ethylene glycol, propylene glycol,
methanol, and salicylates.

Signs and symptoms:

Generally the signs and symptoms are non specific. The respiratory
center gets stimulated and tries to compensate by removing excess
carbon dioxide from the body. Therefore the following signs may be
seen:

Increased ventilation
Dyspnoea
Chest pain

Other signs are as follows:

Palpitations
Headache, fatigue, and confusion
Nausea, vomiting, appetite loss

Management:
The management of metabolic acidosis depends upon two factors –
the severity and the cause.
Severe acidosis (pH < 7.15), irrespective of the cause, is generally
corrected by alkali therapy. This involves intravenous administration
of sodium bicarbonate. 50 to 100 ml ampules of sodium bicarbonate
(containing 50-100 mEq NaHCO3), is added to one litre solution of
5% dextrose or 0.25% normal saline, and is administered over 30 to
45 minutes. Serum electrolytes, must be monitored throughout as
alkali therapy can result in hypernatremia or hypokalemia.

The goal of alkali therapy is not to achieve normal pH, but to bring
the pH to 7.2. Further correction is better achieved by correction of
the underlying cause. Continuous alkali therapy can have adverse
effects such as volume overload, and increased PaCO2, especially
in patients with respiratory dysfunction. In lactic acidosis, it can even
exacerbate the acidosis by stimulating phosphofructokinase, and
must therefore be used with caution in these patients.
Cause – based treatment:

Diabetic ketoacidosis : Insulin therapy.

Starvation and alcohol related acidosis: Intravenous
glucose
Salicylate toxicity: Gastric lavage with saline, followed by
activated charcoal
Ethylene glycol/ methanol toxicity: Saline osmotic diuresis,
antidote such as fomepizole.

METABOLIC ALKALOSIS
This condition is associatedwith an increase in serum bicarbonate
levels.This is generally associated with hypochloremia and
hypokalemia.

Causes:

Based on the amount of chloride that is lost by the body, it can be

categorized as chloride responsive alkalosis and chloride resistant
alkalosis.
Causes of chloride responsive alkalosis:

Loss of gastric HCl – vomiting, nasogastric suctioning

Ingestion of excessive antacids
Loop diuretics and thiazide diuretics.
 Causes of chlride resistant alkalosis:

Hyperaldosteronism
Renin increase – tumors
Autosomal recessive syndromes – Bartter syndrome,
Gitelman syndrome
Hypokalemia, Hypomagnesemia

Signs and symptoms:

These are non-specific and may include:

Weakness
Myalgia
Arrythmias
Depression of ventilation – as a compensatory
mechanism, to retain carbon dioxide.

Management:

If the alkalosis is chloride responsive, it may be corrected

by intravenous infusion of isotonic sodium chloride.
Potassium chloride is preferred if hypokalemia is present
or edema is present.
Vomiting/Gastric suction: Use of H2blockers or proton
pump inhibitors to minimize hydrogen ion losses
Diuretics: These can be stopped or replaced with
acetazolamide or potassium sparing diuretics.
Chloride resistant alkalosis must be treated based on the
cause. Aldosteronism and rennin increase due to tumors
must be corrected by surgery. Dexamethasone therapy
may be used to suppress the HPA axis. Syndromes are
corrected with potassium supplementation and ACE
inhibitors, and potassium sparing diuretics.
Severe alkalosis (pH> 7.55) may require administration of
HCl. Patients in advanced renal failure must additionally
undergo dialysis.
RESPIRATORY ACIDOSIS

Respiratory acidosis occurs when there is alveolar hypoventilation.

The lungs are unable to excrete the excess carbon dioxide, leading
to an increase in PaCO2.
Respiratory acidosis may be of two types – acute and chronic. In
acute acidosis, the pH is low and PaCO2 is high. In chronic acidosis,
the renal system tries to compensate for the acidity by retaining
bicarbonate. This will reflect a normal pH, but causes elevated
serum bicarbonate.

Causes:

Acute respiratory acidosis:

Airway obstruction in acute phases of Asthma or COPD

Respiratory muscle paralysis: Myasthenia gravis, Guillian
Barre syndrome

Chronic respiratory acidosis:

Obstructive sleep apnoea

Severe asthma or COPD
Intersitial fibrosis
Chest wall deformities

Signs and Symptoms:

Dyspnoea
Anxiety
Disturbed sleep, daytime sleepiness
As CO2 content of the blood increases – confusion and
delirium is seen, called carbon dioxide narcosis.
Arterial blood gases show hypoxia as well as
hypercapnoea, and decreased pH.

Management:
As is the case with other acid-base disorders, treatment is aimed at
correcting the underlying respiratory disease. Respiratory ventilation
may be improved by the use of:

Bronchodilators –salbutamol, ipratropium bromide,

theophylline etc.
Respiratory stimulants such as medroxyprogesterone.
Oxygen supplementation –to correct hypoxia.

In life threatening cases, endotracheal intubation and mechanical

positive pressure ventilation must be used to excrete carbon dioxide
from the system.

RESPIRATORY ALKALOSIS

This is caused by an increase in alveolar ventilation, which causes

excess of carbon dioxide to be excreted from the body. As with
acidosis, this can also be acute (high pH) or chronic (normal pH) in
which the kidneys have compensated by excreting bicarbonate,
leading to low serum levels.

Causes:

Centrally – due to stimulation of respiratory center:

Fear and anxiety (commonest cause)

Stroke
Head injury
Drugs and toxins – progesterone, analeptics etc.

Pulmonary stimulation – asthma, pulmonary embolism,

pneumonia

Signs and Symptoms:

Sweating
Fast, shallow breathing
Palpitations, tremors
Management:
Since this condition is usually caused by anxiety, calm reassurance
is an important aspect of treatment.
Patients are asked to rebreathe into a paper bag. This causes them
to inhale more carbon dioxide, thereby increasing the blood levels.

Patients who do not respond may be administered sedatives or

narcotic drugs. Beta adrenergic blockers can help reduce the
adrenergic effects such as palpitations.

SUMMARY:

Any change in the pH of the blood can result in acidosis or

alkalosis.
Metabolic acidosis and alkalosis are the result of either
decreased or increased levels of bicarbonate in the body.
Respiratory acidosis and alkalosis are the result of either
increase or decrease in the partial pressure of carbon
dioxide in the body.
As the symptoms of these disorders are non-specific,
diagnosis is generally made by arterial blood gases, and
anion gap measurement.
The primary treatment should be aimed at correcting the
underlying cause of acidosis or alkalosis.
Severe metabolic acidosis may be corrected by infusion of
sodium bicarbonate, while severe metabolic alkalosis may
be corrected by administering hydrochloride.
Respiratory acidosis is corrected by assisting ventilation
and providing positive pressure ventilation.
Respiratory alkalosis is corrected by rebreathing carbon
dioxide and administering sedatives if required.
REFERENCES:

1. Reddy P, Mooradian AD. Clinical utility of anion gap in

deciphering acid-base disorders. Int J Clin Pract. 2009
Oct. 63(10):1516-25

2. Effros RM, Wesson JA. Acid-Base Balance. Mason RJ,

Broaddus VC, Murray JF, Nadel JA, eds. Murray and
Nadel's Textbook of Respiratory Medicine. 4th ed.
Philadelphia, PA: Elsevier Saunders; 2005. Vol 1: 192-93

3. Kraut JA, Madias NE. Lactic Acidosis: Current Treatments

and Future Directions. Am J Kidney Dis. 2016 Sep. 68
(3):473-82

4. Gennari FJ. Pathophysiology of metabolic alkalosis: a new

classification based on the centrality of stimulated
collecting duct ion transport. Am J Kidney Dis. 2011 Oct.
58(4):626-36

5. Cham GW, Tan WP, Earnest A, Soh CH. Clinical

predictors of acute respiratory acidosis during
exacerbation of asthma and chronic obstructive
pulmonary disease. Eur J Emerg Med. 2002 Sep.
9(3):225-32

6. Gardner WN. The pathophysiology of hyperventilation

disorders. Chest. 1996 Feb. 109(2):516-34
EXERCISES:

1. A high anion gap is seen in which one of the following

conditions?

a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis

2. Which value remains normal in uncompensated metabolic

acidosis?

a. pH
b. Bicarbonate
c. Partial pressure of carbon dioxide
d. None of the above

3. Which of the following is a compensatory mechanism for

metabolic alkalosis?

a. Increased bicarbonate
b. Decreased bicarbonate
c. Increased pCO2
d. Decreased pCO2

4. What is the mainstay of treatment in all acid-base

disorders?

a. Infusing sodium bicarbonate

b. Infusing hydrochloric acid
c. Wait and observe
d. Correct the underlying cause

5. Metabolic acidosis may be associated with which one of

the following electrolyte disturbances?

a. Hyperchloremia
b. Hypochloremia
 c. Hypernatremia
d. Hyponatremia

6. Saline osmotic diuresis is the recommended treatment for

which cause of metabolic acidosis?

a. Diabetic ketoacidosis
b. Ethylene glycol toxicity
c. Salicyate toxicity
d. Lactic acidosis

7. Sodium bicarbonate therapy is given for metabolic

acidosis when the pH falls below which level?

a. 7.25
b. 7.15
c. 7.35
d. 7.45

8. Excessive ingestion of antacids may lead to which one of

the following acid base disorders?

a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis

9. Daytime sleepiness and confusion is a sign of which of the

following abnormalities?

a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis

10. What is the recommended treatment for respiratory

alkalosis?

a. Rebreathing oxygen
b. Rebreathing carbon dioxide
c. Normal breathing
d. None of the above
 CHAPTER VI : SODIUM - HOMEOSTASIS
AND IMBALANCES
As discussed in the earlier chapters, electrolytes form an important
component of body fluids. Therefore, fluid regulation does not
involve the regulation of water alone, individual electrolytes must
also be regulated. The regulation of sodium and chloride, and, to a
lesser extent, potassium, is closely interlinked with fluid regulation, in
order to maintain osmolarity. Incorrect osmolarity would cause cells
to shrink or swell, both of which can damage cellular integrity.

REGULATION OF PLASMA SODIUM :

Sodium has several important roles in the human body. It plays an

important role in the regulation of blood pressure. It is important for
impulse transmission in proper functioning of nerves and muscles.
Since sodium is the main solute in extracellular fluid, its regulation is
very important in order to maintain osmolarity. The normal level of
sodium in the serum is maintained at 135-145 mEq/L. Regulation of
sodium within this range is achieved by several ways, which are
outlined below :

The renin-angiotensin system:

The juxtaglomerular cells of the kidney can detect the

sodium concentration of the renal tubular fluid, as it
passes through the proximal convoluted tubule, and
Henle’s loop.
If there is a lowering of plasma sodium concentration,
these cells detect it and release an enzyme called renin
into the bloodstream.
Renin acts on a plasma protein called angiotensinogen,
and converts it into angiotensin I.
 The pulmonary capillaries secrete another enzyme, the
angiotensin converting enzyme (ACE). When the blood
containing angiotensin I passes through the lungs, ACE
acts on angiotensin I and converts it into angiotensin II.

Angiotensin II stimulates the adrenal cortex to release a

hormone called aldosterone.
Aldosterone acts on the distal convoluted tubule and
collecting duct of the kidney. It causes exchange of
potassium for sodium ions in the renal tubular fluid. Thus
sodium ions are reabsorbed and potassium ions are
excreted.

The adrenal cortex can also directly sense plasma

osmolarity, and cause direct release of aldosterone when
needed.
Another hormone, called atrial natriuretic peptide (ANP) is
released by the heart in high sodium states. It causes
increased excretion of sodium by the kidneys.

IMBALANCE OF SODIUM IN THE BODY

HYPONATREMIA:
Hyponatremia occurs when the plasma sodium concentration falls
below 135 mEq/L. Depending on the amount of decrease in the
sodium concentration, hyponatremia may be mild (130-134 mEq/L),
moderate (125-129 mEq/L), or severe (< 125 mEq/L).
Causes:

Hyponatremia may or may not be associated with a change in total

body water and other solutes. Depending on the osmolarity of the
extracellular fluid, hyponatremia may be hypertonic, normotonic, or
hypotonic. Depending on the water content, it may be classified as
hypovolemic, euvolemic, or hypervolemic hyponatremia.
 Hypertonic hyponatremia: In this, the total body sodium is
normal. However, due to the increased presence of other
osmotically active solutes, sodium gets forced from the
extracellular to intracellular compartment. This may be

seen in diabetes (increased glucose), or administration of

drugs such as mannitol .

Normotonic hyponatremia: This is seen in patients who

have abnormally high levels of lipids or proteins, which
prevents the sodium levels from being measured.
Hypotonic hyponatremia: This may be of three types:

Hypovolemic: Both free water and solute content

are reduced. This is seen in:

Renal disease: polycystic kidney disease,

interstitial nephropathy etc.
Cerebral salt wasting disorders: subarachnoid
hemorrhage, infectious meningitis, carcinoma
etc.
Diuretic drugs, particularly thiazide diuretics.

Hypervolemic: This is usually associated with

clinical edema. Examples: Liver cirrhosis,
congestive cardiac failure, nephritic syndrome

Normovolemic: This is usually seen in hospitalized

patients after major surgery, trauma, or infection. It
is associated with syndrome of inappropriate
antidiuretic hormone secretion (SIADH).

Signs and symptoms:

Tiredness, lethargy, and malaise

 Nausea

Headache
Depressed consciousness

Seizures, coma

Management:
Hyponatremia is a serious condition that must be managed promptly
to prevent cerebral edema. The treatment must follow guidelines
given by the expert committee panel on hyponatremia. These
recommendations are outlined below:

Acute hyponatremia cases (which have a duration of 24-

48 hours) must undergo urgent correction.

For patients who have severe symptoms, who are at

higher risk of neurological damage, 100 ml of 3% sodium
chloride must be infused intravenously over ten minutes.

This can be repeated as needed, up to three times.

In patients with mild to moderate symptoms, the infusion
rate may be reduced to 0.5 – 2 ml/kg/hr.

In cases with a chronic presentation, (duration of more

than 48 hours), correction must be done at a slower rate
to avoid the osmotic demyelination syndrome (ODS),
which can cause necrosis of cells in the pontine region of
the brain.

The infusion rate of such cases must be 4-8 mmol/L in 24

hours.
In patients with SIADH, treatment includes fluid restriction,
increased intake of solutes, and treatment with loop
diuretics must be done.
 In hypovolemic cases, fluid requirement must also be
balanced.

HYPERNATREMIA:
Hypernatremia occurs when the plasma sodium concentration rises
above 145 mmol/L. Generally this occurs when there is a decrease
in the water content of the extracellular fluid relative to the sodium
content. Hypernatremia due to true sodium increase is very rare. The
hyperosmolarity of the extracellular fluid tends to draw water out of
the intracellular compartment, leading to cell shrinkage. This is
particularly significant in neuronal cells and can lead to brain
damage. The low volume of the ECF (due to water loss) can also
have circulatory consequences, such as hypotension and
tachycardia.

Causes:

Factors causing increased loss of water. This is seen in

cases of dehydration due to lack of access, increased
sweating etc.
Renal fluid loss in excess of electrolytes: loop diuretic
drugs, diabetic osmotic diuresis, acute tubular necrosis.

Diabetes insipidus: this is a condition of ADH deficiency, in

which water cannot be reabsorbed.

Impaired thirst mechanism

Signs and symptoms:

These are similar to the signs of dehydration discussed previously.

Cognitive dysfunction – lethargy, confusion, irritability,

seizures

Tachycardia, decreased blood pressure

Dry skin and mucous membranes

Management of hypernatremia:

The management of hypernatremia depends on the

duration of symptoms.

Acute hypernatremia (clinical onset of less than 24 hours)

must be corrected rapidly.
Chronic hypernatremia (>24 hours, usual clinical onset
greater than 48 hours) requires slow correction. This is
because, in chronic hypernatremia, certain amount of
adjustment would have taken place, especially in the brain
cells. Water from intracellular compartment would have
moved extracellularly to maintain volume, leading to
higher intracellular osmotic pressure. In this scenario, if
fluids are rapidly infused, the water would rush into the
cells, leading to cellular edema and demyelination.

Therefore, in acute hypernatremia, a rate of 2 - 3

mEq/L/hr is generally used, up to a maximum of 12
mEq/L/day. On the other hand, in chronic hypernatremia,
the rate of infusion must be restricted to 0.5 mEq/L/hr, and
the total must not exceed 8 – 10 mEq/L/day.

The amount of fluid to be infused depends on the patient’s

total body water, and the amount of sodium present in the
fluid that is used for infusion.
Patient’s total body water is calculated by multiplying the
patient’s body weight with the correction factor. Correction
factors are listed in Table 1.

TABLE 1 . CORRECTION FACTOR VALUES FOR TOTAL BODY

WATER

AGE GROUP MALE FEMALE

Children 0.6 0.6

Young adults 0.6 0.5

Elderly 0.5 0.45

The fluid to be infused is chosen depending on the

amount of sodium that it contains. For instance, 5%
dextrose contains no sodium, 0.2% sodium chloride
contains 34 mmol/L, and 0.45% sodium chloride contains
77 mmol/L.
The change in serum sodium concentration for one liter of
infused fluid is calculated as follows: the difference
between infused sodium and serum sodium is calculated.
This is divided by total body water+ 1 (1 being the water
volume added by infusion). This change in sodium
concentration can guide the volume of fluid that is to be
infused in a single day.
Although the above method is standard, there is a great
deal of interindividual variation. Both the clinical signs and
laboratory values must be monitored during treatment.
Neurological examination must be done periodically, and if
an improvement in clinical signs is seen, the rate of
infusion may be reduced. Serum and urine electrolytes
must also be assessed every 1-2 hours.
The cause of hypernatremia must also be determined and
corrected simultaneously. Better water access, better
control of diabetes mellitus, etc. are some examples.
Hypernatremia die to diabetes insipidus must be corrected
by synthetic ADH (vasopressin).

SUMMARY:
Sodium is the most significant electrolyte that contributes
to plasma osmolarity. It is also essential for muscle and
nerve function.
Regulation of sodium is largely done through the rennin-
angiotensin-aldosterone pathway.
There are several causes for hyponatremia, and it may be
associated with changes in water and other solutes of the
extracellular fluid.
Prompt treatment of hyponatremia must be done to
prevent cerebral edema. 3% hypertonic saline is given for
treatment.
Hypernatremia usually occurs with dehydration. It must be
corrected by infusion of fluids that are low in sodium.
For both hyponatremia and hypernatremia, chronic cases
must be corrected slowly to prevent irreversible brain
damage.
REFERENCES:

1. Fried LF, Palevsky PM. Hyponatremia and hypernatremia.

Med Clin North Am. 1997 May. 81(3):585-609

2. Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C,

Schrier RW, Sterns RH, et al. Diagnosis, evaluation, and
treatment of hyponatremia: expert panel
recommendations. Am J Med. 2013 Oct. 126 (10 Suppl
1):S1-42

3. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med.

2000 May 25. 342(21):1581-9.

4. Hoorn EJ, Zietse R. Diagnosis and Treatment of

Hyponatremia: Compilation of the Guidelines. J Am Soc
Nephrol. 2017 May. 28 (5):1340-1349

5. Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med.

2000 May 18. 342(20):1493-9.

6. Lindner G, Schwarz C, Kneidinger N, et al. Can we really

predict the change in serum sodium levels? An analysis of
currently proposed formulae in hypernatraemic patients.
Nephrol Dial Transplant. 2008 Nov. 23(11):3501-8

7. Muhsin SA, Mount DB. Diagnosis and treatment of

hypernatremia. Best Pract Res Clin Endocrinol Metab.
2016 Mar. 30 (2):189-203
EXERCISES:

1. What is the most important role of sodium in the body?

a. It increases bone strength

b. It is an integral part of the neuromuscular network
c. It aids the continuous pumping of the heart
d. It plays a role in acid base balance

2. What hormones affect sodium concentration?

a. Adrenaline and testosterone

b. Aldosterone and testosterone
c. Aldosterone and anti-diuretic hormone
d. Adrenaline and anti-diuretic hormone

3. What is the earliest sign of sodium deficiency?

a. Headache
b. Abdominal pain
c. Fatigue
d. Seizures

4. What organ does aldosterone signal to control sodium

levels?

a. Lungs
b. Skin
c. Kidneys
d. Adrenal gland

5. How does our body routinely excrete sodium?

a. Through the urine

b. Through bowel movement
c. Through the saliva
d. Through the skin
 6. Which signs and symptoms are not associated with
sodium excess?

a. Lethargy
b. Seizures
c. Confusion
d. Insomnia

7. What are the consequences of rapid correction of

hypernatremia?

a. Cerebral edema
b. Pulmonary edema
c. Generalized edema
d. Peripheral edema

8. Increased excretion of sodium in the urine is facilitated by

which one of the following?

a. Adrenaline
b. Anti-diuretic hormone
c. Atrial natriuretic peptide
d. Angiotensin

9. What fluid is used for infusion in patients with

hyponatremia?

a. 0.9% sodium chloride

b. 0.25% sodium chloride
c. 2% sodium chloride
d. 3% sodium chloride

10. Synthetic vasopressin must be used for correction of

which of the following causes of hypernatremia?

a. Renal tubular necrosis

b. Diabetes mellitus
c. Diabetes insipidus
d. Juvenile diabetes
 CHAPTER VII : CHLORIDE - HOMEOSTASIS
AND IMBALANCES
Chloride is a negatively charged ion which can combine with cations
in the body such as sodium and hydrogen ions. Along with sodium, it
plays an important role in maintaining the osmotic pressure of body
fluids. It forms a key component of the digestive acid of the stomach
(hydrochloric acid). It also interacts with other ions in the body during
the regulation of acid base balance. The normal blood level of
chloride is 97-108 mmol/l

REGULATION OF CHLORIDE IN THE BODY:

Chloride regulation generally occurs parallel to regulation of sodium.

The levels are regulated by balancing dietary intake with the amount
that is excreted and reabsorbed by the kidneys. Unlike sodium,
reabsorption of chloride is a passive process. In the proximal
convoluted tubule, initially there is active reabsorption of sodium and
water, followed by various other solutes. This causes an increase of
chloride concentration on the tubular fluid as compared to plasma,
by the time the fluid reaches the end of the proximal convoluted
tubule. Owing to the difference in this concentration, chloride gets
reabsorbed into the plasma. However, in the collecting duct, chloride
either gets absorbed or secreted in exchange for bicarbonate ions.
The amount would be determined by the existing chloride levels in
the body.

IMBALANCES:
HYPOCHLOREMIA:

This occurs when the chloride level goes below 97 mmol/L.

Hypochloremia can lead to alkalosis, because, chloride ions are
generally exchanged for bicarbonates in the renal tubules. In the
absence of chloride, bicarbonates are retained, which increase the
alkalinity of the blood.
Causes:

Inadequate dietary intake

Defective renal tubular absorption
Excessive loss – vomiting, diarrhea, especially chloride
losing diarrhea in children, excessive nasogastric tube
suctioning.

Signs and Symptoms:

Hypochloremia generally does not present with specific signs and
symptoms. However, in infants who have hypochloremic alkalosis,
the following features may be seen:

Vomiting and watery diarrhea

Failure to thrive
Lethargy, confusion, and seizures

Muscle weakness and cramps

Abdominal distention

Management:

Since hypochloremia rarely occurs in isolation, the patient

must be assessed for dehydration, hyponatremia, and
hypokalemia.

In cases which appear to be severe (patient in shock),

aggressive fluid resuscitation must be started with isotonic
fluids, preferably 0.9% sodium chloride. If hypokalemia is
present, potassium chloride may be added.

Serum electrolytes must be reassessed after 6 hours in

order to calculate maintenance.
 If hypochloremia is due to gastrointestinal cause, such as
acid reflux or pyloric stenosis, surgical intervention must
be done.

Mild cases of hypochloremia may be corrected by

increasing the dietary intake alone.

HYPERCHLOREMIA:

Hyperchloremia occurs when the serum chloride level rises above

107 mmol/L. It is usually associated with acidosis, as, increased
levels of chloride are seen only when bicarbonates are deficient.
Causes:

Dehydration

Excessive intake of salt/sea water

Cystic fibrosis
Congestive cardiac failure

Metabolic acidosis

Signs and Symptoms:

Nausea, tiredness

Mental confusion progressing to stupor

Tachypnoea may be present if there is an attempt at
respiratory compensation.

Management:
The management of hyperchloremia would depend on the cause.

Excess ingestion must be corrected by withholding further

salt intake.
 Metabolic acidosis is corrected by bicarbonate infusion.

Dehydration is treated by water replenishment.

SUMMARY:

Chloride is the predominant anion of the extracellular fluid,

and along with sodium, maintains the osmolarity of the
ECF.

Chloride homeostasis is passive and parallels sodium

homeostasis. The amount of chloride excreted and
reabsorbed is passively adjusted based on serum levels.
Since chloride indirectly affects acid-base balance,
hypochloremia can cause alkalosis, and hyperchloremia
can cause acidosis.

Hypochloremia is treated by infusion of isotonic saline.

Hyperchloremia is treated by water replenishment and

withholding further chloride ingestion.
REFERENCES:

1. Berend, K., van Hulsteijn, L., & Gans, R. (2012). Chloride:

The queen of electrolytes?. European Journal Of Internal
Medicine, 23(3), 203-211.

2. Galla, J. (1988). Chloride Transport And Disorders Of

Acid-Base Balance. Annual Review Of Physiology, 50(1),
141-158.

3. Tani, M., Morimatsu, H., Takatsu, F., & Morita, K. (2012).

The Incidence and Prognostic Value of Hypochloremia in
Critically Ill Patients. The Scientific World Journal, 2012,
1-7.

4. Al-Abbad A, Nazer H, Sanjad SA, Al-Sabban E. Congenital

chloride diarrhea: A single center experience with ten
patients. Ann Saudi Med. 1995 Sep. 15(5):466-9

5. Nagami, G. (2016). Hyperchloremia – Why and how.

Nefrología, 36(4), 347-353.
EXERCISES:

1. What is the approximate normal value for serum chloride?

a. 87 -97 mmol/l
b. 97 – 107 mmol/L
c. 107 – 117 mmol/ L
d. 117- 127 mmpl/L

2. Reabsorption of chloride occurs parallel to which other

electrolyte?

a. Potassium
b. Sodium
c. Magnesium
d. Calcium

3. Which of the following is not a treatment for

hypochloremia?

a. Sodium chloride
b. Potassium chloride
c. Calcium chloride
d. Dietary chloride

4. Which of the following signs is not seen in a

hypochloremic patient?

a. Vomiting
b. Bone pain
 c. Muscle cramps
d. Lethargy

5. Which of the following is not a cause for hyperchloremia?

a. Dehydration
b. Inadequate dietary intake
c. Cystic fibrosis
d. Congestive cardiac failure
 CHAPTER VIII : POTASSIUM -
HOMEOSTASIS AND IMBALANCES
Potassium is an important electrolyte that plays an important role in
multiple functions of the body. It is primarily an intracellular cation. It
plays an important role in determining the resting membrane
potential of the cell and maintains intracellular osmotic balance. It is
crucial for several enzyme activities, and plays an important role in
cell growth and division. Besides this, potassium has a key role to
play in maintenance of acid-base balance in the body.

REGULATION OF POTASSIUM:

Potassium is acquired by the body primarily though dietary intake.

90% of body potassium is excreted through urine, while the
remaining 10% is excreted through feces. Most of the potassium
acquired by the body is taken up by the cells, and only 2% remains
in the extracellular fluid. However, if there is a decrease in the ECF
concentration of potassium for any reason, the cells release
potassium in order to maintain this balance.
Renal excretion of potassium occurs at various levels. While
potassium is filtered out initially by the glomeruli, about 2/3rd is
reabsorbed passively at the level of the proximal convoluted tubule.
Some amount of potassium gets secreted in the descending loop of
Henle and gets reabsorbed again in the thick ascending loop.
However, the final determinant of the amount of potassium to be
excreted takes place at the distal convoluted tubule and collecting
duct. There is active secretion which is regulated by the hormone
aldosterone.
The cells of the zona glomerulosa of the adrenal cortex are sensitive
to changes in serum potassium levels. If the serum potassium is
high, the adrenal cortex releases aldosterone, which in turn acts on
the distal convoluted tubule and collecting duct and causes
increased secretion of potassium into the tubular fluid. Similarly, if
the serum potassium is low, the secretion of aldosterone and hence
excretion of potassium is suppressed.

The normal serum value of potassium is 3.5 - 5.2 mmol/L. The body
is extremely sensitive to changes in potassium, and even small
changes can have major manifestations. These changes are detailed
below.

HYPOKALEMIA

Hypokalemia occurs when the serum potassium level falls below 3.5
mmol/L. Depending on the value of decrease, it may be categorized
as mild hypokalemia (3.0 – 3.5 mmol/L), moderate (2.5 – 3.0
mmol/L), or severe hypokalemia (less than 2.5 mmol/L).
Causes:

Inadequate dietary intake: In elderly patients, patients with

eating disorders such as anorexia and bulimia etc.
Excessive excretion of potassium:

Adrenal tumors that produce excess aldosterone

Uncontrolled diabetes: Excess glucose in the blood
can cause osmotic dieresis
Drugs causing increased excretion: Diuretics,
mannitol
Gastrointestinal losses: Vomiting, diarrhea.
Autosomal recessive disorders associated with
increased potassium excretion: e.g. Bartter
syndrome, Gitelman syndrome, Gullner syndrome
etc.

Potassium shift: Sometimes potassium can shift from the

extracellular to intracellular compartment, causing low
serum levels. This may be seen in alkalosis, hypothermia,
and refeeding conditions (e.g. starvation), and with some
drugs such as insulin and beta-agonists.
Signs and Symptoms :

Patients with mild hypokalemia usually do not show signs and

symptoms. There may be some weakness, tiredness, and fatigue,
but the patient rarely automatically associates this with low
potassium levels.
Most symptoms are related to muscle function and cardiac function.
These may be:

Muscle pain and cramping

Palpitations
Severe cases – bradycardia and collapse of the
cardiovascular system.
Neurological signs may be seen in severe cases –
hallucinations, delirium, psychosis etc.

Management:
The aim of management of hypokalemia is twofold – identifying the
cause for potassium loss, in order to minimize or stop it, and to
replenish the body’s existing potassium stores.
Stopping the cause:

Any diuretic, laxative, or other drug that is suspected of

causing hypokalemia must be discontinued immediately.
Potassium sparing diuretics are a feasible alternative.
For potassium deficit due to gastrointestinal loss, drugs
must be administered to stop diarrhea and vomiting.
Patients who are receiving nasogastric tube suctioning
must be placed on H2 blockers.
In uncontrolled diabetics, glucose levels must be brought
under control to prevent potassium loss due to polyuria.
Surgical intervention may be required to remove the
cause in certain cases, such as adrenal adenomas.

Replenishment of potassium:
 In mild and moderate hypokalemia, replacement may be
done through oral fluids.
Severe hypokalemia requires immediate intravenous
potassium.
This must be done at a slow rate of 10 mEq/hour.
Potassium replacement should be followed closely with
ECG monitoring throughout.
Serum potassium levels should be measured periodically
to avoid potential hyperkalemia.

HYPERKALEMIA
Hyperkalemia occurs when the serum potassium rises beyond 5.0
mmol/L. Hyperkalemia is a serious condition that can escalate
quickly in severity and have fatal consequences. Hence, it must be
identified and managed promptly. When unmanaged, hyperkalemia
can lead to cardiac arrest and death.

Causes:

Increased intake of potassium:

Dietary intake – this is especially common with ‘salt

substitutes’ which contain large quantities of
potassium
Intravenous infusion: during hypokalemia correction
Intravenous infusion of drugs such as penicillin G or
packed red cells.

Decreased excretion of potassium:

Renal diseases that affect the distal tubule of

kidney. These include diabetic nephropathy, and
urinary tract obstruction.
Addison’s disease and Genetic disorders

Shift of potassium from the intracellular space into

extracellular space: This can occur in cell death such as
 tumor lysis or muscle lysis, metabolic acidosis, toxicity of
chemotherapeutic drugs such as methotrexate and
cyclosporine.

Signs and Symptoms:

Just like hypokalemia, there could be little to no symptoms for
hyperkalemia. The reported symptoms are usually vague and are
related to muscle function or cardiac function. These can include:

Weakness and fatigue

Tingling of the skin
Palpitations and chest pain
Nausea, vomiting

Any patient who is suspected of having hyperkalemia must have an

ECG in addition to serum and urine potassium testing. This is
because false positives for hyperkalemia in blood tests are common.
Blood cells may rupture, releasing the potassium from the
intercellular fluid to the blood stream.

The ECG changes depend on the level of rise of potassium.

Mild rise (5.5 – 6.5 mEq/L): QT interval is shortened, T

waves are tall and peaked, and ST segment is inverted.
Moderate increase (6.5 – 8 mEq/L): shows decreased or
absent P waves, PR interval is prolonged, QRS interval is
widened, R wave is amplified, and T wave is peaked.
High increase (>8.0 mEq/L): shows absence of P wave,
QS is widened, and conduction blockade is seen. In later
stages, patterns of ventricular fibrillation or even asystole
may emerge.

Management:
The management depends on the severity of hyperkalemia.

Mild to moderate hyperkalemia:

 If the patients do not have any cardiac symptoms and
ECG abnormalities, aggressive management is not
required.
Diuretics may be administered to promote excretion of
potassium.
If necessary, cation exchange resins may be
administered. These are small beads which allow
exchange of potassium for hydrogen ions.

Severe hyperkalemia:
This must be managed aggressively. There are three arms of
treatment for severe hyperkalemia:

Prevention of cardiac toxicity:

Intravenous calcium administration protects the heart muscle

from arrhythmias and arrest.

Increasing potassium uptake by cells:

This is done by administering insulin and glucose infusion.

Insulin tends to increase potassium uptake by the cells.

Increasing potassium excretion by the kidneys :

Loop diuretics may be administered. This must be done only if

the renal function is normal.
In emergency cases, potassium may be removed by dialysis.

Other measures:

If the patient is in metabolic acidosis, it must be corrected with

bicarbonates or beta adrenergic agonists.

SUMMARY:

Potassium is the predominant intracellular cation, and it

plays an important role in intracellular osmolarity,
maintaining resting membrane potential, and acid-base
balance.
Potassium levels in the serum are largely controlled by
aldosterone.
Hypokalemia may be mild, moderate, or severe, and may
be caused by decreased intake, excessive excretion, or
intracellular shift of potassium.
It is managed by correcting the cause, and replenishing
the body stores with intravenous potassium, at 10 mEq
per hour.
Hyperkalemia occurs mostly with renal dysfunction, or
massive cell lysis.
It can have serious cardiac effects, and calcium gluconate
must be given to protect the heart. Excess potassium can
be removed with diuretics, or by dialysis.
REFERENCES:

1. Marino PL. Potassium. The ICU Book. Baltimore:

Williams & Wilkins; 1998

2. Palmer BF. Regulation of Potassium Homeostasis. Clinical

Journal of the American Society of Nephrology : CJASN.
2015;10(6):1050-1060.

3. Greenlee M, Wingo CS, McDonough AA, Youn JH, Kone

BC. Narrative review: evolving concepts in potassium
homeostasis and hypokalemia. Ann Intern Med. May
2009. 150:619-625

4. Chew HC, Lim SH. Electrocardiographical case. A tale of

tall T's. Hyperkalaemia. Singapore Med J. 2005 Aug.
46(8):429-32

5. Gumz ML, Rabinowitz L, Wingo CS. An Integrated View of

Potassium Homeostasis. N Engl J Med. 2015 Jul 2. 373
(1):60-72
EXERCISES:

1. Where are most of our potassium reserves stored?

a. extracellular fluids
b. intracellular fluids
c. plasma
d. bones

2. Which of the following is not a function of potassium?

a. Maintaining resting membrane potential

b. Contributes to acid-base balance
c. Aids in blood clotting
d. Main contributor to intracellular osmolarity

3. What is the normal concentration of potassium in the

blood?

a. 0.1-0.3 millimoles per liter

b. 3.0-7.2 millimoles per liter
c. 3.5-5.2 millimoles per liter
d. 5.5-6.0 millimoles per liter

4. What is an example of the signs and symptoms of

hypokalemia?

a. Muscle pain
b. Weakened bones
c. Hallucinations
d. Palpitations

5. Intracellular shift of potassium may be seen in all except:

a. Refeeding syndrome
b. Starvation
c. Renal failure
d. Insulin therapy
6. What infusion is given to drive potassium into the cells?

a. Insulin
b. Glucose
c. Both the above
d. Neither of the above

7. In which part of the kidney is potassium reabsorbed?

a. Proximal convoluted tubule

b. Descending loop of Henle
c. Ascending loop of Henle
d. Distal convoluted tubule

8. Hyperkalemia is caused by all the following except:

a. Excess dietary intake of salt substitutes

b. Addison’s disease
c. Infusion of packed cells
d. Drugs like diuretics
 CHAPTER IX : CALCIUM - HOMEOSTASIS
AND IMBALANCES
Calcium is the most abundant cation present in the body as it forms
most of the body’s skeletal framework in the form of calcium
phosphate. However, it has a limited concentration in the intracellular
and extracellular fluids. Calcium has multiple uses in the body. Most
people know of its importance maintaining the integrity and strength
of bones. It also helps in activation of several proteins, including
clotting factors in the blood. It is important for the proper functioning
of nerves. Calcium levels in the extracellular fluid determine the
sensitivity of voltage gated sodium ion channels. Low levels can
cause hyperexcitability and high levels can cause depression of
nerves. It serves as a secondary messenger for cell signaling. It also
plays an important role in muscle contraction.

REGULATION OF CALCIUM:
Calcium enters the body through dietary intake and gets excreted
through urine and feces. A large portion of calcium that enters the
body is taken up by the bones, the rest exists in the body fluids.

The normal value of calcium in the extracellular fluid is around 2.2 –

2.6 mmol/L. This exists in two forms. Approximately half of this exists
in the free or ionized form (1.1 – 1.3 mmol/L). This form is
biologically active. The remainder, which is biologically inactive,
exists in a bound form to various proteins and sulphates, the most
common protein being albumin.
Dietary calcium is absorbed from the small intestine under the
influence of Vitamin D (calcitriol). Excess calcium in the body is
excreted by the kidneys, under the influence of the parathyroid
hormone. The bones of the body act as reservoirs of calcium ions in
the body, and can take up calcium ions from the blood or secrete
them in to the blood as needed.
The level of ionized calcium in the plasma has to be set within
extremely narrow limits in order to avoid excitation or depression of
nerves. This is achieved by the action of two hormones – parathyroid
hormone (PTH) which is secreted by the parathyroid gland, and
calcitonin, which is secreted by the parafollicular cells of the thyroid
gland.

When the blood levels of ionized calcium are higher than usual, the
following actions take place:

Calcitonin secretion increases, which in turn causes the

bones to take up calcium from the blood into storage.
PTH secretion is suppressed, which in turn has the
following effects:

Inhibition of the removal of calcium from the bones.

Increased excretion of calcium in urine.
Decreases the excretion of phosphate in urine. This
increases blood levels of phosphate, which combine
with calcium, thereby decreasing the concentration
of ionized calcium.
Also inhibits the activation of Vitamin D
(Chlolecalciferol to calcitriol), which has two actions
– it prevents further intestinal absorption of calcium,
and inhibits bone osteoclasts from releasing calcium
into the blood.

If the level of ionized calcium in the blood falls below normal limits,
the following actions take place:

PTH secretion is stimulated, which has the following

effects:
Bone is stimulated to release calcium into the blood
Decreased excretion of calcium, and increased excretion
of phosphate in urine.
Vitamin D is activated, leading to more intestinal
absorption of calcium
 Calcitonin secretion is suppressed, which prevents the
bone from taking up calcium.

IMBALANCES:
HYPOCALCEMIA:

Hypocalcemia occurs when the total blood calcium level falls below 2
mmol/L. This may be a fall in ionized calcium alone (‘true’
hypocalcemia) or may reflect a fall in the unionized portion of
calcium.
Causes:

Deficiency of parathyroid hormone: Primary or secondary

hypoparathyroidism, pseudoparathyroidism.
Vitamin D deficiency: Rickets, osteomalacia
Hypoalbuminemia: malnutrition, sepsis, burns etc.
Disorders of other electrolytes such as
hyperphosphatemia or hypomagnesemia
Systemic diseases: Hepatic disease (impairs albumin),
renal disease (impairs Vitamin D activation) etc.
Drugs: Antiepileptic drugs, foscarnet etc.
Following gastric surgery: impairs calcium absorptio n

Signs and Symptoms:

Earliest symptoms are numbness and tingling sensations

Muscle spasms can occur. Classic manifestation is
carpopedal spasm, referred to as tetany.
Laryngospasm and bronchospasm may occur, leading to
wheezing and breathlessness
Irritability and depression
Later stages – seizures
Signs of hypocalcemia:

Chvostek sign: Tapping the skin over the facial

nerve causes ipsilateral contraction of the facial
 nerve muscles.
Trousseau’s sign: A blood pressure cuff is used on
the upper arm and inflated 20mmHg above systolic
pressure. There is flexion at the wrist and
metacarpo-phalangeal joints.

Management:

In cases of mild hypocalcemia, oral calcium

supplementation is all that is required. The cause must be
identified and corrected. Serum levels of parathyroid
hormone and Vitamin D must be analyzed and corrected.
Severe hypocalcemia, which presents with tetany,
seizures or arrhythmias, must be corrected with
intravenous calcium. Calcium gluconate or calcium
chloride is infused over 5 to 10 minutes.
The serum levels must be monitored regularly to avoid
overcorrection. In cases where the cause is
hypoalbuminemia, ionized calcium must be measured
separately.
In chronic cases, regular calcium supplementation must
be taken, along with supplements of Vitamin D and
adequate exposure to sunlight.

HYPERCALCEMIA:

This occurs when the blood levels of calcium rise beyond 2.5
mmol/L. This can be due to either impaired excretion of calcium by
the kidneys, or due to too much calcium entering the blood from the
bone reservoirs. Hypercalcemia may be categorized as mild (2.5 –
3.0 mmol/L), moderate (3.0 – 3.5 mmol/L), and severe, also called
hypercalcemic crisis (more than 3.5 mmol/L)

Causes:

Malignancies: This is seen in bone metastases, that cause

increased osteoclastic activity, and tumors that secrete
parathyroid hormone related peptide.
 Hyperparathyroidism: Tumors or hyperplasia of the
parathyroid gland
Vitamin D toxicity.
Other conditions that cause high turnover of bone.

Signs and Symptoms:

Hypercalcemia affects several organs of the body; clinical
manifestations are produced accordingly. This is popularly described
as ‘stones, bones, abdominal moans, and psychic groans’. These
are described in detail below:

Renal manifestations: Excess calcium can lead to the

formation of renal calculi. This can cause dehydration,
pain in the lower abdomen, and even renal failure.
Gastrointestinal manifestations: Nausea, vomiting,
constipation, and gastric ulcers.
Central nervous system manifestations: Lethargy,
confusion, depressed consciousness.
Cardiac manifestations: Since calcium is believed to have
a positive inotropic effect, excess calcium in the blood can
cause arrhythmias.

Management:

Management of hypercalcemia depends on the cause and the

severity.

Medical management:

Isotonic sodium chloride can flush out excess calcium

temporarily and is good for short-term management
Loop diuretics – increase calcium excretion
Bisphosphonate drugs – prevent osteoclastic activity
Dialysis: both peritoneal dialysis and hemodialysis are
effective in immediately lowering serum calcium levels.

Surgical management:
 Tumors responsible for raised calcium levels must be
resected.
Primary hyperparathyroidism requires surgical removal of
the parathyroid glands.

SUMMARY:

Calcium is an important cation that makes up the body’s

structural framework. It also acts as a secondary
messenger and is essential for muscle contraction.
Calcium homeostasis is regulated by the interaction
between Vitamin D, parathyroid hormone, and calcitonin
Hypocalcemia is mainly caused by Vitamin D deficiency,
or impaired PTH secretion or function.
It is manifested by numbness, muscle spasms such as
carpopedal spasm, Chvostek’s sign and Trousseau’s sign
It is treated by oral or intravenous calcium
supplementation.
Hypercalcemia is due to malignancies or Vitamin D
toxicity. It manifests with renal stones, bone pain, and
gastric pain.
Treatment is by diuretics, dialysis, and bisphosphonate
drugs.
REFERENCES:

1. Mundy GR, Guise TA. Hormonal control of calcium

homeostasis. Clin Chem. 1999 Aug. 45(8 Pt 2):1347-52

2. Cooper MS, Gittoes NJ. Diagnosis and management of

hypocalcaemia. BMJ. 2008 Jun 7. 336(7656):1298-302

3. Goyal A, Bhimji SS. Hypocalcemia. [Updated 2017 Apr

25]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2017 Jun-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK430912

4. Goldner W. Cancer-Related Hypercalcemia. J Oncol Pract.

2016 May. 12 (5):426-32.

5. Makras P, Papapoulos SE. Medical treatment of

hypercalcaemia. Hormones (Athens). 2009 Apr-Jun.
8(2):83-95

6. Turner JJO. Hypercalcaemia - presentation and

management . Clin Med (Lond). 2017 Jun. 17 (3):270-273
EXERCISES:

1. Where are most of our calcium reserves stored?

a. Blood
b. Muscle tissues
c. Bones
d. Intracellularly

2. All the following are functions of calcium, except:

a. Bone metabolism
b. Muscle contraction
c. Clotting of blood
d. Regulation of body temperature

3. What is the normal concentration of calcium in the blood?

a. 0.2-0.9 millimoles per liter

b. 2.2-2.6 millimoles per liter
c. 6.0-10.0 millimoles per liter
d. 10.0 -12.0 millimoles per liter

4. What is the condition where there is an increased levels of

calcium in the blood?

a. Hypocalcemia
b. Hypercalcemia
c. Hypercalci uria
d. Hypocalciuria

5. What is an example of the signs and symptoms of

hypocalcemia?

a. Loss of appetite
b. Muscle spasm
c. Hair loss
d. Increase in body temperature
6. Chvostek sign is used to stimulate which of the following
nerves?

a. Facial nerve
b. Optic nerve
c. Trigeminal nerve
d. Glossopharyngeal nerve

7. Which is not a treatment modality for hypercalcemia?

a. Hypotonic saline
b. Bisphosphonates
c. Loop diuretics
d. Dialysis

8. Which organ system is not affected by hypercalcemia?

a. Renal system
b. Cardiovascular system
c. Respiratory system
d. Gastrointestinal system
CHAPTER X : MAGNESIUM - HOMEOSTASIS
AND IMBALANCES
Magnesium is the second most abundant intracellular cation, after
potassium. It acts as a cofactor for several enzymes, and therefore
plays an important role in cellular processes such as transcription of
DNA, synthesis of proteins, and energy metabolism. It is necessary
for bone formation, as part of hydroxyapatite, and also for regulation
of muscle contraction.

REGULATION OF MAGNESIUM BALANCE:

The normal level of magnesium in the blood is 0.7 -1.1 mmol/L.

Magnesium balance is maintained in the body by coordination of
function between the intestine, bones, and kidneys.

The source of magnesium for the body is through dietary intake,

which is usually around 30 mg per day. Magnesium absorption is
carried out by the cells of the small intestine. Most of the absorption
is passive, through transcellular transport. If the dietary intake
increases, active absorption takes place, though paracellular
transport. Proton pump inhibitors can decrease absorption of
magnesium from the small intestine .
About 50% of body magnesium is stored in the bones. It is also
stored in muscle and soft tissue. When the blood levels are lowered,
magnesium is released from these sources.

The kidney filters almost 2000 mg of magnesium per day. However,

most of this is reabsorbed. 10-30% of magnesium gets reabsorbed
in the proximal convoluted tubule, 40-70% of magnesium gets
reabsorbed in the thick ascending loop of Henle, and 5 to 10% gets
reabsorbed in the distal convoluted tubule.
There are several factors which can affect renal reabsorption of
magnesium.
Increased reabsorption of magnesium:

Hormones – parathyroid hormone, calcitonin, glucagon,

insulin, aldosterone
Metabolic alkalosis
Epidermal growth factor

Decreased reabsorption of magnesium:

Increased blood levels of calcium and magnesium

Prostaglandin E2
Metabolic acidosis
Drugs – diuretics, antibiotics, immunosupressants

IMBALANCES:
HYPOMAGNESEMIA

This occurs when the plasma magnesium level falls below 0.7
mmol/L. Hypomagnesemia is an important condition that can cause
disturbances in virtually every organ system in the body. It has been
associated with several systemic diseases and can cause other
electrolyte disturbances as well .
Causes:

Reduced dietary intake of magnesium: starvation,

intravenous total parenteral nutrition, or alcoholism
Reduced absorption of magnesium by the small intestine:
drugs such as proton pump inhibitors
Shift of magnesium from the extracellular to intracellular
space: refeeding syndromes, diabetic ketoacidosis, and
alcohol withdrawal syndrome.
Increased excretion: due to decreased reabsorption of
magnesium from the thick ascending loop of Henle and
distal convoluted tubule. This can occur in several
conditions, described in the previous section on
 magnesium regulation, and also in autosomal recessive
disorders such as Gilteman’s syndrome.

Signs and symptoms:

Weakness, fatigue, lethargy

Numbness
Hyper-reflexes
Muscle cramps and tetany
Convulsions
Nausea, vomiting
Arrythmias
ECG changes are seen, which include T wave changes,
prolonged QT interval, and abnormal patterns of
ventricular tachycardia, ventricular fibrillation, or torsades
de pointes.

Consequences:
Magnesium deficiency has been implicated in several systemic
diseases, such as:

Hypertension
Diabetes
Coronary artery disease
Osteoporosis
Renal stones and nephrolithiasis

Sudden magnesium deficit can have fatal consequences due to

ventricular arrhythmias and coronary artery vasospasm.

It is also associated with other electrolyte imbalances such as:

Hypokalemia: due to increased excretion of potassium

Hypocalcemia: this is secondary due to impaired PTH
release.

Management:
 Mild cases can be corrected by increasing the dietary
intake alone.
Oral replenishment for chronic cases. This includes oral
intake of magnesium oxide, or magnesium chloride, at a
dose of 60-80 mg (3.5 mmol), at least six to eight times a
day.
Acute and life threatening cases must undergo
intravenous replacement. 50 mEq of magnesium can be
given over 8 to 24 hours, until the blood level reaches at
least 0.4 mmol/L.
It is important to monitor serum levels of potassium and
calcium, and correct these if required.

HYPERMAGNESEMIA:
Hypermagnesemia occurs when the serum magnesium levels cross
1.2 mmol/L. However, symptoms occur only if the serum level
crosses 2 mmol/L, and the manifestations increase in severity with
increasing levels.

Causes:

Increased ingestion of magnesium: Due to over-the-

counter medications such as Epsom salts, antacids, and
laxatives that contain high amounts of magnesium.
Excess iatrogenic administration: During management of
conditions associated with hypomagnesemia.
Renal failure: prevents normal excretion of magnesium
Tissue breakdown that releases intracellular magnesium
ions into the blood: sepsis, burns

Signs and symptoms

Neuromuscular manifestations:
Absence or depressed deep tendon reflexes
Muscle weakness and paralysis (above 5 mmol/L)
Facial paresthesia
Respiratory muscle weakness- apnea
 Decreased cardiac conduction – bradycardia, heart block,
and even cardiac arrest (above 7 mmol/L)
Bleeding: prevents platelet activation and thrombin
generation, thereby prolongs bleeding

Management:

To prevent cardiac toxicity: Intravenous calcium gluconate

is given.
To remove excess magnesium from body: Diuretics such
as furosemide are used, or dialysis may be done.
Promote intracellular uptake: A combination of glucose
and insulin infusion will help to drive magnesium ions into
the cells.

SUMMARY:

Magnesium is an important intracellular cation that is a

cofactor for enzymes, and is involved in DNA
transcription, protein, and energy metabolism.
Homeostasis of magnesium is regulated by several
hormones including parathyroid hormone, calcitonin,
insulin, aldosterone, and epidermal growth factor.
Hypomgnesemia affects every organ system in the body
and plays a role in pathogenesis of several systemic
diseases.
It may be corrected by dietary intake, oral supplements, or
intravenous supplements.
Hypermagnesemia is mainly caused by antacid overdose,
especially Epsom salt.
Therapy includes protecting the heart with calcium
infusion, using diuretics and dialysis, and driving
magnesium intracellularly with insulin-glucose.
REFERENCES:

1. Glasdam SM, Glasdam S, Peters GH. The Importance of

Magnesium in the Human Body: A Systematic Literature
Review. Adv Clin Chem. 2016. 73:169-93

2. Blaine, J., Chonchol, M., & Levi, M. (2014). Renal Control

of Calcium, Phosphate, and Magnesium Homeostasis.
Clinical Journal Of The American Society Of Nephrology,
10(7), 1257-1272.

3. Weber, C., & Santiago, R. (1989). Hypermagnesemia.

Chest, 95(1), 56-59. De Baaij, J. H. F., Hoenderop, J. G. J.,
& Bindels, R. J. M. (2012). Regulation of magnesium
balance: lessons learned from human genetic disease.
Clinical Kidney Journal, 5(Suppl 1), i15–i24.

4. Martin KJ, González EA, Slatopolsky E. Clinical

consequences and management of hypomagnesemia. J
Am Soc Nephrol. 2009 Nov. 20(11):2291-5

5. Bringhurst FR, Demay MB, Krane SM, et al. Bone and

mineral metabolism in health and
disease/hypermagnesemia. Kasper DL, et al, eds.
Harrison's Principles of Internal Medicine. 16th ed. New
York, NY: McGraw-Hill; 2005. 2245
EXERCISES:

1. What is the normal level of magnesium in the blood?

a. 0.7 – 1.1 mmol/l

b. 1.7 – 2.1 mmol/l
c. 2.7 - 3.1 mmol/l
d. 3.7 - 4.1 mmol/l

2. Magnesium is stored in all except which one of the

following body tissues?

a. Bone
b. Muscle
c. Soft tissue
d. Blood

3. In which part of the kidney does maximum magnesium

reabsorption take place?

a. Proximal convoluted tubule

b. Loop of Henle
c. Distal convoluted tubule
d. Collecting duct

4. Which of the following hormones is not involved in the

regulation of magnesium?

a. Aldosterone
b. Insulin
c. Adrenaline
d. Calcitonin

5. Which of the following factors causes decreased

reabsorption of magnesium?

a. Parathyroid hormone
b. Epidermal growth factor
c. Metabolic alkalosis
 d. Prostaglandin E2

6. What is the normal intravenous dose of magnesium for

correction of hypomagnesemia?

a. 20 mEq
b. 30 mEq
c. 40 mEq
d. 50 mEq

7. All the following are systemic diseases that are associated

with low magnesium levels, except:

a. Osteoporosis
b. Diabetes mellitus
c. Rheumatoid arthritis
d. Hypertension

8. Which of the following electrolytes can show

abnormalities with hypomgnesemia?

a. Sodium and potassium

b. Potassium and calcium
c. Calcium and sodium
d. Calcium and phosphorous

9. The following are signs and symptoms associated with

hypermagnesemia, except:

a. Hyper reflexes
b. Facial paresthesia
c. Bradycardia
d. Bleeding

10. The management of hypermagnesemia involves all of the

following, except:

a. Calcium gluconate therapy

b. Diuretics
c. Intravenous magnesium
d. Insulin- glucose infusion
 CHAPTER XI : PHOSPHOROUS -
HOMEOSTASIS AND IMBALANCES
Phosphorous is a prominent intracellular anion and has several
important functions. It contributes to the structural integrity of cells as
a component of the cell membrane and nucleic acids. It forms the
end product and reservoir of energy metabolism (Adenosine
triphosphate or ATP), and it activates several enzymes by
phosphorylating them. It plays an important role in maintaining acid-
base balance of the body, and contributes to bone mineralization.

REGULATION OF PHOSPHOROUS LEVELS:

The normal blood level of phosphorus is 0.8 to 1.45 mmol/L.

Phosphorous is acquitted through dietary sources, which should
ideally be around 1000mg to 1500 mg per day. Absorption primarily
takes place in the jejunum area of the small intestine. Some amount
of phosphorous also gets secreted into the intestine by the bile and
pancreatic juice, which is then absorbed from the intestine.
Phosphorous absorption takes place both passively, through
diffusion, and actively, through sodium dependent transporters
(NaPiIIa, NaPiIIb, and NaPiIIc). Vitamin D (calcitriol) plays an
important role in enhancing phosphorous absorption from the small
intestine .

In the body, phosphorous is stored primarily in the bones and teeth,

and to a certain extent in soft tissues. There is a need-based
movement of phosphorous between the bone cells and blood.
Whenever bone mineralization takes place, phosphorous is taken up
from the blood stream, and whenever there is resorption of bone,
phosphorous is released into the bloodstream.
Excretion of phosphorous takes place primarily through the kidneys.
This is completely filtered at the glomerular level, and is reabsorbed
in the proximal convoluted tubule. The amount of phosphorous
reabsorbed in the proximal tubule is negatively dependent on
parathyroid hormone. High PTH expression decreases reabsorption
and low levels stimulate reabsorption.

Another group of regulators, called phosphatonins, are believed to

regulate the metabolism of phosphorous. Of these, the phosphatonin
which has been scrutinized closely is the fibroblast growth factor-23
(FGF-23), whose expression is believed to be increased with
increased dietary intake of Vitamin D. FGF-23, like PTH, also
decreases renal reabsorption of phosphorous, and promotes
excretion. It is believed to suppress calcitriol activity, and, to a lesser
extent, PTH.
FGF-23, calcitriol, and PTH are all interrelated as follows:

Calcitriol stimulates expression of FGF-23

FGF-23 suppresses both calcitriol, and PTH.
PTH stimulates calcitriol.

HYPOPHOSPHATEMIA

Hypophosphatemia is a condition where the phosphate levels in the

blood fall below 0.8 mmol/L .
Causes:

Inadequate intestinal absorpttion: Although uncommon, it

may occur in Vitamin D deficiency, poor diet, and
excessive intake of antacids.
Increased excretion: Hyperparathyroidism, Phosphate
wasting syndromes such as Fanconi syndrome.
Shift from the extracellular to intracellular space:
Refeeding syndrome, diabetic ketoacidosis, respiratory
alkalosis etc.

Signs and symptoms:

These are extremely non-specific. Mild cases are not symptomatic.

Symptoms may be seen in severe cases or long standing cases.
These include:
 Weakness
Bone pain
Rhabdomyolysis: muscle breakdown and pain.
Altered mental status

If the phosphate imbalance is not managed well and blood

phosphate levels continue to go down, the patient may experience
some psychological effects. Some patients may experience
increased irritability and confusion. Some patients also show slurred
speech.
If left unmanaged, the patient may have chest pains and cardiac
dysrhythmia. It will be followed by increased breathing rate. In worst
cases, the condition may lead to seizures and coma.

Management :

The best way to deal with low phosphate levels is to reintroduce the
electrolyte back in the system. In hospitals and other medical
facilities, this can be done with intravenous potassium phosphate.
This is done to people whose phosphate levels are severely low, or
in life threatening situations, such as hypocalcemia with tetany,
hyperkalemia, and metabolic acidosis .
For those who have mild hypophosphatemia, oral phosphate
supplements may also be used. This is also used in places where
intravenous methods are not available.

Supportive therapy, such as Vitamin D supplementation, and

concomitant correction of calcium and potassium imbalances, is
essential to treatment of hypophosphatemia.

As with other electrolyte imbalances, hypophosphatemia will

continue unless the underlying condition is addressed.
The ideal modality of management is outlined in the table below:

TABLE 1. MANAGEMENT OF HYPOPHOSPHATEMIA

 SEVERITY OF BLOOD MODALITY OF
HYPOPHOSPHATEMIA LEVELS MANAGEMENT

Severe – critically ill < 0.3 mmol/L Intravenous

patients, and phosphate infusion,
0.3 – 0.8 at a rate of 0.08 to
Moderate – in ventilated mmol/L 0.16 mmol/kg, over 2
patients – 6 hours

Moderate – in non- 0.3 – 0.8 Oral phosphate

ventilated patients, and mmol/L supplementation
alone
Mild 0.8 mmol/L

HYPERPHOSPHATEMIA
Hyperphosphatemia is said to occur when the serum phosphate
concentration exceeds 1.46 mmol/L. It is usually, but not always
associated with hypercalcemia.

Causes:

Excessive intake: either through diet or intravenous

therapy
Shift from intracellular to extracellular space: This occurs
when cells are destroyed.

Crush injuries
Rhabdomyolysis
Hemolytic anemia
Drugs – Chemotherapeutic agents, which are
cytotoxic etc.
 Metabolic or respiratory acidosis: tends to shift
phosphorous between cells
Decreased excretion of phosphorous:

Hypoparathyroidism or resistance to PTH in Vitamin

D toxicity, or magnesium imbalance.
Renal failure or insuffieciency

Signs and symptoms

Initially, hyperphosphatemia is asymptomatic, or presents with
vague, nonspecific symptoms.

Fatigue, weakness
Nausea, vomiting, anorexia
Shortness of breath
Disturbances in sleep and insomnia.

Later on, signs of hypocalcemia may manifest, including the

following:

Trousseau’s sign and Chvostek’s sign

Carpopedal spasms
Hyper-reflexes
Seizures and convulsions.

Management:

The cause must be identified in order to administer correct

treatment.
Intake of dietary phosphate must be restricted .

Patients can take medications that bind with phosphorous and

thereby reduce their blood levels. Phosphate binders are compounds
that limit the absorption of phosphate from food, and need to be
taken with each meal. As it travels through the gastrointestinal tract,
the active agent in the drug binds with the protein. They are excreted
with the food eaten because the bound phosphate is insoluble.
There are several types of phosphate binders. Lanthanum carbonate
and Sevelamer compounds are preferred. Calcium and aluminium
based binders are also available, but are generally avoided as they
can carry their own side effects.

If the cause of hyperphosphatemia is tumor lysis, and if the renal

function is intact, saline diuresis can be done to wash off excess
phosphate from the body.
In cases of renal dysfunction, hemodialysis may be used for removal
of excess phosphorous from the body.

SUMMARY:

Phosphorous is an intracellular cation, that is important for

structural integrity of the cell and cell components.
Homeostasis of phosphorous is achieved by regulation
between Vitamin D, parathyroid hormone, and
phosphatonins like FGF-23
Hypophosphatemia is usually associated with
hypercalcemia and hyperphosphatemia is associated with
hypocalcemia.
Hypophosphatemia occurs with Vitamin D deficiency and
hyperparathyroidism. It can be managed by oral
supplementation, intravenous being reserved for severe
cases.
Hyperphosphatemia occurs when parathyroid hormone
secretion is reduced or resistance develops, or during cell
lysis
Depending on the cause, it is managed with phosphate
binder, saline diuresis or dialysis.
REFERENCES:

1. Penido, M. G. M. G., & Alon, U. S. (2012). Phosphate

homeostasis and its role in bone health. Pediatric
Nephrology (Berlin, Germany), 27(11), 2039–2048.

2. Bergwitz, C., & Jüppner, H. (2010). Regulation of

Phosphate Homeostasis by PTH, Vitamin D, and FGF23.
Annual Review of Medicine, 61, 91–104.

3. Liamis G, Milionis HJ, Elisaf M. Medication-induced

hypophosphatemia: a review. QJM. 2010 Jul. 103(7):449-
5

4. Block GA, Wheeler DC, Persky MS, et al. Effects of

phosphate binders in moderate CKD. J Am Soc Nephrol.
2012 Aug. 23(8):1407-15
EXERCISES:

1. What is the normal range of phosphate in the blood?

a. about 0.8 to 1.4 mmol/L

b. about 0.2 to 0.8 mmol/L
c. about 0.3 to 0.5 mmol/L
d. about 0.6 to 2.5 mmol/L

2. Absorption of phosphate takes place in:

a. Duodenum
b. Jejunum
c. Ileum
d. Colon

3. Which of the following is an example of Phosphatonin?

a. Calcitriol
b. Epidermal growth factor 23
c. Fibroblast growth factor 23
d. Parathyroid hormone

4. Which of the following statements is true?

a. Calcitriol depresses expression of FGF-23

b. FGF-23 suppresses both calcitriol, and PTH.
c. FGF-23 stimulates both calcitriol, and PTH.
d. PTH depresses calcitriol

5. Which serum level of phosphate indicates severe

hypophosphatemia?

a. Less than 0.8 mmol/L

b. Less than 0.7 mmol/L
c. Less than 0.5 mmol/L
d. Less than 0.3 mmol/L
 6. Which one of the following is a sign or symptom of
hypophosphatemia?

a. Itchiness of the skin

b. Bone pain
c. Shortness of breath
d. Bloating of extremities

7. How is mild Hypophosphatemia treated?

a. Phosphate supplements
b. Phosphate binders
c. Taking diuretics
d. Dialysis

8. Intravenous supplementation of phosphorus is indicated

in which one of the following situations?

a. Moderate hypophosphatemia in non- ventilated

patients
b. Moderate hypophosphatemia in ventilated patients
c. Mild hypophosphatemia
d. Intravenous supplementation is never indicated

9. In which of the following situations can

hyperphosphatemia occur?

a. Metabolic acidosis
b. Respiratory acidosis
c. Both of the above
d. Neither of the above

10. Which of the following is preferred as phosphate binder?

a. Lanthanum compounds
b. Calcium compounds
c. Aluminum compounds
d. Strontium compounds
 CHAPTER XII : IMBALANCES IN COMMON
MEDICAL CONDITIONS
Now that an overview has been provided into fluid and electrolyte
imbalances, it would have been noted that the cause of most of
these imbalances is similar. Generally, dysfunction of any one of the
major organ systems, or insult to the body as a whole would bring
about changes in the normal homeostatic mechanisms, leading to
fluid, electrolyte, and acid-base disorders. These disorders would
occur in combination, rather than in isolation. A few of the common
medical conditions in which these would present are described in
this chapter.

HYPERTHERMIA:
Hyperthermia, or heat stroke, is a condition where the body heats up
because thermoregulation fails. This can occur in the presence of
excessive environmental heat, excessive exertion, or a combination
of both.

Pathophysiology of imbalances:

Heat causes the body to lose more fluid, both through

sweat and insensible losses. Therefore, the patient
develops dehydration.
As fluid loss occurs, the concentration of electrolytes
relatively increases. This can lead to hypernatremia.
Hypokalemia is seen in early heat stroke due to fluid and
electrolyte redistribution. However, in later phases, as
muscle damage increases, potassium is released from
damaged cells leading to hyperkalemia.
Hypocalcemia and hypomagnesemia are observed,
secondary to other electrolyte disturbances.
Lactic acidosis may occur because of poor aerobic
metabolism and accumulation of lactates.
Management:

Immediate cooling of the body is the mainstay of

treatment, and can halt or reverse the disease process.
This is accomplished by ice water immersion, or
evaporative cooling therapy.
Infusion of dextrose with sodium bicarbonate can provide
fluid resuscitation, drive potassium intracellularly, and
counter acidosis.
Calcium must be used only if cardiac signs develop.

CARDIAC FAILURE:
Cardiac failure occurs when the heart muscle is unable to pump
sufficient blood to meet the requirements of the entire body. The
various neurohumoral adaptive mechanisms that take place in heart
failure, as well as the various drugs used, can contribute to
electrolyte and acid-base disorders.

Pathophysiology of imbalances:

Hyponatremia: when the cardiac output decreases, the

renal blood flow and hence glomerular filtrate also
decreases, leading to water retention. Apart from this,
there is activation of renin-angiotensin mechanism as well
as the ADH hormone, which leads to more retained water,
thereby diluting the sodium content present.
Hypokalemia: this can occur secondary to renin-
angiotensin activation, and can also be a consequence of
diuretic therapy. Hypokalemia is a strong predictor of
mortality rate as by itself, it can cause cardiac arrhythmias
in these patients.
Hypomagnesemia: although this is commonly observed in
patients with heart failure, its pathophysiology is less well
understood. It is believed to be due to reduced dietary
intake, renal losses due to diuretics, and due to
redistribution of other electrolytes.
 Hypocalcemia and hypophosphatemia: These do not
always occur, but may be seen sometimes secondary to
other electrolyte disturbances.
Acid-base disturbances: Usually these patients can
present with metabolic alkalosis, sometimes in
combination with respiratory alkalosis. This is mainly due
to loss of hydrogen ions in the urine, and driving of
hydrogen ions intracellularly. Hypoxia, due to reduced
circulating blood, is also a contributing factor.

Management:

Since cardiac failure is a condition with high morbidity,

focus is usually on treating the condition proper. Based on
the severity, treatment for heart failure ranges from
pharmacological therapy and revascularization
procedures, to a total heart transplant.
At every stage on therapy, however, the electrolytes and
blood gases must be analyzed periodically, so that drug
therapy may be modified, and any electrolyte imbalances
may be corrected.
It is especially important to keep potassium and
magnesium levels within their normal ranges, as these
electrolytes play an important role in heart health.

RESPIRATORY DISEASE:

Respiratory failure occurs when the lungs fail to facilitate exchange

of carbon dioxide for oxygen. This leads to lack of oxygen (hypoxia)
and excess of carbon dioxide (hypercapnea) in the body.

Pathophysiology of imbalances:

Since the respiratory mechanism of acid-base

homeostasis is suppressed, there is accumulation of
carbon dioxide in the body. This results in respiratory
acidosis due to raised PaCO2.
 Impaired lung function can eventually cause pulmonary
edema and right heart dysfunction, which in turn affects
the renin-angiotensin-aldosterone axis, and stimulates
ADH release. The net effect is water retention, leading to
hyponatremia.

Management:

The mainstay of therapy is correcting the hypoxemia. The

standard of treatment is extracorporeal membrane
oxygenation, which reverses the hypoxia, and thereby the
hypercapnea.
Once these abnormalities are reversed, electrolytes must
be monitored and corrected if required.
Severe acidosis may require assisted mechanical
ventilation to remove carbon dioxide from the body.

GASTROINTESTINAL FLUID LOSSES:

There are several instances where fluid may be lost from the
gastrointestinal tract. While gastric fluid is acidic, the bile and
pancreatic juice secretions are more alkaline. Thus the electrolyte
and acid-base imbalance would depend on the type of fluid that is
lost .

Pathophysiology of imbalances:

Vomiting and diarrhea leads to fluid loss, along with loss

of sodium and potassium. This is further exacerbated by
inadequate intake. Generally this manifests as
hypokalemia and hypochloremia. Hypochloremia results in
alkalosis.
On the other hand in conditions like pancreatic fistulae,
loss of pancreatic juice can cause losses of bicarbonate,
along with sodium and potassium, leading to a net
acidosis.
Milk alkali syndrome: This is seen in peptic ulcer patients
who have ingested large quantities of antacids. This is
 associated with hypercalcemia and mild alkalosis.
Magnesium levels may also be raised.
Steatorrhoea is a condition where there is impaired fat
absorption. This also impairs the absorption of calcium
and phosphorous, leading to hypocalcemia and
hypophosphatemia.

Management:
Management depends on the cause of gastric fluid losses.
Electrolyte monitoring according to the trends mentioned above is
essential. Management must be tailored to meet the abnormality.

RENAL FAILURE:

Renal failure invariably causes electrolyte abnormalities across the

entire spectrum, and can result in complex acid-base disturbances.
Pathophysiology of imbalances:

Since there is failure of fluid excretion, there is fluid

excess, leading to edema. Although sodium is also
retained, the excessive fluid retention results in a net
dilution and hyponatremia.
Hyperkalemia: failure of secretion of potassium in the
renal tubule.
Kidneys are also responsible for activation of vitamin D,
which in turn influence calcium levels. In renal failure,
hypocalcemia and hyperphosphatemia is frequently
encountered.
In renal failure, magnesium fails to get excreted, leading
to hypermagnesemia.
Renal failure also prevents reabsorption of bicarbonate,
resulting in metabolic acidosis.

Management:
The cause of renal failure must be determined and managed if
possible.

Diuretic drugs are frequently used to remove excess water

and electrolytes. However, this must be done with caution
as diuretic therapy itself can lead to electrolyte
imbalances. Electrolyte monitoring is done frequently and
drugs must be modified or changed as needed.
Dialysis, both hemodialysis and peritoneal dialysis, are the
mainstay of treatment and remove excess electrolytes.
Oral bicarbonate supplementation is helpful in cases of
chronic kidney failure. Calcium supplementation can be
done orally or intravenously.

BURNS:
Pathophysiology of imbalances:

Below the large necrotic area of the burn, inflammatory mediators

are released.
These cause increase in vascular permeability, causing plasma to
shift out of vessels into the interstitial and intracellular space,
causing cell edema. Both sodium and water are shifted intracelluarly.

Early phase:

Hyponatremia: due to extracellular sodium depletion

Hyperkalemia: released during cell damage of burnt area.
Acidosis : secondary to hyperkalemia

Second phase:

Hypernatremia: mobilization of intracellular sodium,

activation of rennin-angiotensin pathway
Hypocalcemia: due to potassium losses and intracellular
shift
Hypomagnesemia and hypophosphatemia: due to loss of
other electrolyes
Management:

First the hyperkalemia is treated:

Calcium chloride infusion to counter cardiac effects

of hyperkalemia
Drive potassium intracellularly with insulin and
glucose infusion

Sodium bicarbonate to correct acidosis if needed

Use of diuretics/dialysis to excrete potassium
If hypernatremia persists, it is corrected with hypotonic
fluids
All other electrolytes – calcium, phosphate, magnesium,
must be observed every few hours and corrected if
needed.

SUMMARY:

Certain medical conditions cause imbalances of several

electrolytes at once. As these symptoms are non-specific,
it is important to be aware of this and monitor electrolytes
periodically.
Hyperthermia causes fluid loss due to heat, leading to
hypernatremia and acidosis.
Congestive cardiac failure causes edema and water
retention, leading to hyponatremia and metabolic alkalosis
Respiratory failure primarily causes respiratory acidosis
Gastric fluid disturbances depend on the nature of fluid
lost. Loss of gastric juice can cause alkalosis while loss of
pancreatic fluid can cause acidosis
Renal failure upsets almost all electrolytes as the kidneys
play an important role in reabsorption of these. Hence all
electrolytes must be monitored and managed periodically.
Burns patients develop increased vascular permeability
and fluid shifts interstitially and intracellularly. This causes
hyponatremia and hyperkalemia. Acidosis can occur.
REFERENCES:

1. Noakes, T. D. (1998). Fluid and electrolyte disturbances in

heat illness. International journal of sports medicine, 19(S
2), S146-S149.

2. Simon, H. B. (1993). Hyperthermia. New England Journal

of Medicine, 329(7), 483-487.

3. Noakes, T. D. (1998). Fluid and electrolyte disturbances in

heat illness. International journal of sports medicine, 19(S
2), S146-S149.

4. Moe, A. E. (1955). Electrolyte Balance in Gastrointestinal

Disease. California Medicine, 83(5), 339–342.

5. Haberal, M., Sakallioglu Abali, A. E., & Karakayali, H.

(2010). Fluid management in major burn injuries. Indian
Journal of Plastic Surgery : Official Publication of the
Association of Plastic Surgeons of India, 43(Suppl), S29–
S36.
EXERCISES:

1. What is not an accepted mode of treatment for

hyperthermia?

a. Ice water immersion

b. Evaporative therapy
c. Warm saline infusion
d. Bicarbonate therapy

2. Which of the following electrolyte abnormalities is not

seen in cardiac failure?

a. Hyponatremia
b. Hypernatremia
c. Hypokalemia
d. Hypocalcemia

3. Respiratory failure causes which one of the following acid

base disorders?

a. Metabolic acidosis
b. Metabolic alkalosis
c. Respiratory acidosis
d. Respiratory alkalosis

4. Which one of the following digestive secretions has an

acidic pH?

a. Saliva
b. Gastric juice
c. Bile
d. Pancreatic juice

5. Renal failure results in which one of the following acid

base disorders?

a. Metabolic acidosis
b. Metabolic alkalosis
 c. Respiratory acidosis
d. Respiratory alkalosis

6. Steathorrhoea would affect the absorption of which of the

following electrolytes?

a. Sodium
b. Potassium
c. Magnesium
d. Calcium

7. In which of the following medical conditions are all the

electrolytes invariably affected?

a. Respiratory disease
b. Hypertension
c. Renal disease
d. Nervous disease

8. In which phase of burns does hyponatremia occur?

a. Early phase
b. Late phase
c. Both phases
d. Hyponatremia does not occur

9. What is the reason for fluid shift in burns patients?

a. Lymphatic block
b. Increased vascular permeability
c. Increased blood pressure
d. None of the above

10. Irrespective of the medical condition, which electrolyte

abnormality must be addressed first?

a. Potassium
b. Sodium
c. Calcium
d. Phosphorous
 CONCLUSION
We hope this book was able to help you to learn about body fluids,
electrolytes and the acid-base balance. By now, you must be familiar
with the normal homeostatic mechanisms in place for regulation of
fluids, electrolytes, and acid-base balance. You must also be familiar
with recognizing the common disorders associated with disturbance
in these homeostatic mechanisms. It must be remembered that
correcting fluid and electrolyte imbalances in patients with these
disorders will go a long way in reducing morbidity and mortality.
This book has outlined the basic management modalities for fluid
and electrolyte disorders. However, it must be remembered that
management of these disorders is often a challenging undertaking
and must be approached with caution. Fluid resuscitation is the
mainstay of therapy, but choice of fluid, and the rate and quantity of
administration, is extremely critical. Rapid correction can lead to
severe complications. Overcorrection can also lead to imbalances of
other electrolytes in the system. Moreover, fluid administration is a
dynamic process, and there is often high inter-individual variability.
Therefore, in managing patients with these disorders, it is necessary
not only to apply knowledge learned in this book, but also to take into
account the patients’ entire systemic condition. It is necessary to
periodically test for levels of not only the electrolyte being corrected,
but other electrolytes as well. As has been emphasized at various
points, correction of the underlying cause is the best modality of
treatment.

The next step is to keep on learning about how the imbalances

discussed in this book affect your own specialization in the medical
field. You should also come back to this book in the future to remind
yourself of how fluid, electrolytes and the acid-base balance are
interconnected. Fluids and electrolytes are often an extremely
volatile subject, which needs constant refreshing in order to deliver
better care. You can repeat the post-chapter exercises at periodic
intervals to assess your memory.
Thank you and good luck !
 ANSWERS TO EXERCISES
CHAPTER I

1. b
2. c
3. b
4. a
5. d
6. c
7. c
8. a
9. c
10. c

CHAPTER II

1. c
2. a
3. c
4. c
5. b
6. d
7. c
8. b
9. b
10. b

CHAPTER III

1. c
2. c
3. b
4. d
5. b
6. c
7. a
 8. d
9. c
10. a

CHAPTER IV

1. c
2. a
3. c
4. d
5. c
6. b
7. d
8. c
9. a
10. b

CHAPTER V

1. a
2. c
3. c
4. d
5. a
6. b
7. b
8. b
9. c
10. b

CHAPTER VI

1. b
2. c
3. c
4. c
5. a
6. d
7. a
 8. c
9. d
10. c

CHAPTER VII

1. b
2. b
3. c
4. b
5. b

CHAPTER VIII

1. b
2. c
3. c
4. a
5. c
6. c
7. d
8. d

CHAPTER IX

1. c
2. d
3. b
4. b
5. b
6. a
7. a
8. c

CHAPTER X

1. a
2. d
3. b
 4. c
5. d
6. d
7. c
8. b
9. a
10. c

CHAPTER XI

1. a
2. b
3. c
4. b
5. d
6. b
7. a
8. b
9. c
10. a

CHAPTER XII

1. c
2. b
3. c
4. b
5. a
6. d
7. c
8. a
9. b
10. a
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