FLUID AND

ELECTROLYTE
BALANCE
DR GEETHU K S
D E PA R T M E N T O F O M F S
 INTRODUCTION

• Claude Bernade coined the term Milieu Interieur

• State of body – interstitial fluid that bathes the cells and plasma
together – maintain normal morphology , function – tissues and cells
in body

• Homeostasis – constancy of internal environment

NORMAL
COMPOSITION
FUNCTIONS OF
ELECTROLYTES
• Acid base balance

• Osmolarity and volume maintainance

• Specific physiologic function

ACID BASE BALANCE
• First line of defence
Buffer
• Most important buffer system is bicarbonate and
system haemoglobin

• Depends on arterial partial pressure of carbon

Pulmona dioxide
ry action

Renal • Most effective buffering mechanism

mechani
sm
BUFFER MECHANISM

Bicarbona
te buffer

Phosphat
Proteins
e buffer
BICARBONATE BUFFER SYSTEM

• 2 ingredients
1. H2CO3
2. NaHCO3

CO2 + H2O → H2C03 → H+ + HCO3-

PHOSPHATE BUFFER
SYSTEM
• ICF and renal tubular fluid

• Main elements are H2PO4- and HPO4=

PROTEIN BUFFER

• Plentyful protein intracellularly

• Most abundant buffer system in body

• Haemoglobin
PULMONARY MECHANISM

• Balances metabolic formation of CO2

• Increased H+ concentration stimulates alveolar

ventillation

• 1-2 times stronger than buffer system

RENAL CONTROL

• For excretion of non volatile gases

• Prevention of loss of bicarbonate in urine

• Both is accomplished by secretion of H+ into renal

tubules
Change in bicarbonate level

Metabol
Metabol
ic
ic
alkalosi
acidosis
s
 Change in PCO2

Respirato Respirato
ry ry
acidosis alkalosis
METABOLIC ACIDOSIS

• acid other than carbonic acid (due to CO2 retention)

accumulates in the body
• Ingestion or infusion of • Aspirin poisoning
inorganic acid • Methanol poisoning
• Gastrointestinal HCO3− • Ethylene glycol
loss poisoning
• Diabetic ketoacidosis • Lactic acidosis
• Starvation ketosis • Kidney disease
• Alcoholic ketoacidosis
CLINICAL FEATURES

• uncontrolled diabetes • associated symptoms,

mellitus such as visual
• kidney failure or shock complaints in methanol
poisoning
• clinical history of
starvation
• Alcoholism
INVESTIGATIONS

• blood gas measurements

• measurements of creatinine, electrolytes and

bicarbonate
MANAGEMENT

• identify and correct the underlying cause

• resuscitation with intravenous fluids

• In alcoholism and starvation ketosis, intravenous

glucose is indicated

• Malnourished patients may also require thiamin,

potassium, magnesium and phosphate supplements
• Use of intravenous bicarbonate is controversial

• rapid correction of acidosis can induce hypokalaemia or

a fall in plasma ionised calcium

• the use of bicarbonate infusions is best reserved for

situations where the underlying disorder cannot be
readily corrected and acidosis is severe
METABOLIC ALKALOSIS

• increase in the plasma bicarbonate concentration and

the plasma pH
CAUSES

• primary • overuse of antacid salts

hyperaldosteronism
(Conn’s syndrome)
• Cushing’s syndrome
• glucocorticoid therapy
• Hypovolaemic metabolic alkalosis is the most common pattern

• sustained vomiting, in which acid-rich fluid is lost directly from

the body

• by treatment with loop diuretics or thiazides

• Normovolaemic (or hypervolaemic) metabolic alkalosis occurs

when bicarbonate retention and volume expansion occur
simultaneously.
MANAGEMENT

• Metabolic alkalosis with hypovolaemia

1. intravenous infusions of 0.9% saline with potassium

supplements
2. reverses the secondary hyperaldosteronism and
allows the kidney to excrete the excess alkali in the
urine

• In metabolic alkalosis with normal or increased volume,

treatment should focus on management of the
underlying endocrine cause
RESPIRATORY ACIDOSIS

• rise in the PCO2, with a compensatory increase in

plasma bicarbonate concentration

• Depression of respiratory centre

• Respiratory obstruction

• Management : correct the underlying cause

RESPIRATORY ALKALOSIS

• develops when there is a period of sustained

hyperventilation, resulting in a reduction of PCO2

• If the condition is sustained, renal compensation occurs,

such that tubular acid secretion is reduced
CAUSES

• Hyperventillation in anxiety

• High altitudes
CLINICAL FEATURES

• agitation associated with perioral and digital tingling -

binding of calcium to albumin- reduction in ionised
calcium concentrations

• Severe cases -Trousseau’s sign and Chvostek’s sign may

be positive, and tetany or seizures
SODIUM HOMEOSTASIS

• Normally, about 80% of sodium is reabsorbed

1. intrinsic renal mechanism

2. extra-renal mechanism

• retention of water is affected by release of antidiuretic

hormone
INTRINSIC RENAL MECHANISM

sudden reduction in the effective arterial blood volume

(hypovolaemia)

stimulates the arterial baroreceptors present in the

carotid sinus and aortic arch

sympathetic outflow via the vasomotor centre in the brain

reduction in the glomerular filtration rate

decreased excretion of sodium in the urine

consequent retention of sodium

EXTRA-RENAL MECHANISM

• secretion of aldosterone, a sodium retaining hormone,

by the renin- angiotensin-aldosterone system

• granular cells in the juxta-glomerular apparatus

secretes renin

• stimulated in response to low concentration of sodium

in the tubules

• main action is stimulation of the angiotensinogen

• Angiotensin 1 to angiotensin II

• Angiotensin II stimulates the adrenal cortex to secrete

aldosterone hormone

• increases sodium reabsorption in the renal tubules and

sometimes causes a rise in the blood pressure.
ADH MECHANISM

• Retention of sodium leads to retention of water

secondarily under the influence of anti-diuretic hormone
(ADH) or vasopressin

• secreted by the cells of the supraoptic and

paraventricular nuclei in the hypothalamus

• stored in the neurohypophysis (posterior pituitary)

• stimulated by increased concentration of sodium in the
plasma and hypovolaemia

• Large amounts of ADH produce highly concentrated

urine.
• The possible factors responsible for causation of
oedema by excessive retention of sodium and water
1. Reduced glomerular filtration rate in response to
hypovolaemia.

2. Enhanced tubular reabsorption of sodium and

consequently its decreased renal excretion

3. Increased filtration factor i.e. increased filtration of

plasma from the glomerulus
• Decreased capillary hydrostatic pressure associated
with increased renal vascular resistance

1. Oedema of cardiac disease e.g. in congestive cardiac

failure.
2. Ascites of liver disease e.g. in cirrhosis of liver.
3. Oedema of renal disease e.g. in nephrotic syndrome,
acute glomerulonephritis.
OEDEMA

• abnormal and excessive accumulation of “free fluid” in

the interstitial tissue spaces and serous cavities
• Free fluid in body cavities
1. as ascites (if in the peritoneal cavity)
2. hydrothorax or pleural effusion (if in the pleural
cavity)
3. hydropericardium or pericardial effusion (if in the
pericardial cavity)
• Free fluid in interstitial space

• oedema in the subcutaneous tissues, momentary

pressure of finger produces a depression known as
pitting oedema

• non-pitting or solid oedema in which no pitting is

produced on pressure e.g. in myxoedema, elephantiasis
• Localised - limited to an organ or limb - lymphatic
oedema, inflammatory oedema, allergic oedema.

• Generalised (anasarca or dropsy) - renal oedema,

cardiac oedema, nutritional oedema.

• special forms of oedema - pulmonary oedema, cerebal

oedema
• transudate which is more often the case, such as in
oedema of cardiac and renal disease

• exudate such as in inflammatory oedema

CARDIAC OEDEMA
PULMONARY OEDEMA
DEHYDRATION

• pure deprivation of water leading to sodium retention

and hence a state of hypernatraemia

• intense thirst, mental confusion, fever, and oliguria.

ETIOLOGY
GI excretion:
1. Severe vomitings
2. Diarrhoea
3. Cholera
Renal excretion
4. Acute renal failure
5. Extesive use of diuretics
6. Endocrine diseases e.g.
diabetes insipidus,
Addison’s disease
Loss of blood and plasma
1. Severe injuries
2. severe burns
3. During childbirth
Loss through skin
4. Excessive perspiration
5. Hyperthermia
Accumulation in third
space
MANAGEMENT

• treat the cause where possible, to stop ongoing salt and

water losses

• replace the salt and water deficits, and provide ongoing

• maintenance requirements, usually by intravenous fluid

replacement when depletion is severe.
OVERHYDRATION

• Excessive unmonitored • Renal retention of

intravascular infusion: sodium and water
1. Normal saline (0.9% 1. Congestive heart
sodium chloride) failure
2. Ringer lactate 2. Acute
glomerulonephritis