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DR AVINASH RATHORE
• Basic Terminologies And Definitions
• Body Fluids And Fluid Balance
• Regulation Of Fluids
• Principals Of Fluid Therapy
• Classification Of I.V Fluids
• Fluids in specific conditions
• Acid – base disorders
• Electrolyte disorders
• Clinical implications
Basic Terminologies And
• Fluid :- [Latin fluidus - flowing freely]
A substance, such as a liquid or gas, that
can flow, has no fixed shape, and offers
little resistance to an external stress
• Electrolyte :
A substance that ionizes when dissolved in
suitable ionizing solvents such as water.
• Osmolality :
Is the amount of solute dissolved in a solvent
measured in weight(per kg of solvent)
Is the amount of solute dissolved in a solvent
measured in volume (per litre of solvent).
• Osmotic Pressure :
Is the distribution of water among the
different fluid compartments,particularly
between ECF & ICF.
• The ability of an extracellular solution to make
water move into or out of a cell by osmosis is
know as its tonicity. A solution's tonicity is
related to its osmolarity, which is the total
concentration of all solutes in the solution.
• RULE OF OSMOLARITY- movement of solvent
from LOW concentration to HIGH
“Intravenous fluids have a range of physiologic effects and
should be considered to be drugs with indications, dose
ranges, cautions, and side effects.”
In 1861 ,Thomas Graham’s investigated and classified
substances as crystalloids and colloids depending on their
ability to diffuse through a parchment membrane.
• Crystalloids are fluids that pass through a semipermeable
• Colloids are fluids that do not pass through semipermeable
• The administration of intravenous (IV) fluid is a
core expertise for surgeons and an area in which
we have an important role in advising clinical
• The aims of IV fluid administration should be to-
– avoid dehydration
– maintain an effective circulating volume
– prevent inadequate tissue perfusion during a period
when the patient is unable to achieve these goals
through normal oral fluid intake.
• Knowledge of the composition and the clinical
effects of different fluids has increased
substantially in recent years.
• The choice of fluid type in a variety of clinical
situations can be rationally guided by an
understanding of the physicochemical and
biologic properties of the various crystalloid and
colloid solutions available in combination with
the available clinical trial data.
Composition of Body Fluids
• Water is the universal solvent
– Electrolytes – Inorganic salts, all acids and
bases,and some proteins.
– Non-electrolytes –Most non electrolytes are
organic molecules – glucose
•Electrolytes have greater osmotic power than non
•Water moves according to osmotic gradients
• Elderly: Have lower % of total body fluid than
• Women: Have lower % total body fluid than
• Infants : Have 80% of body water in relation to
weight and declines with age.
Regulation Of Fluids
• Hypothalmus –Thirst receptors
(osmoreceptors) continuosly monitor serum
osmolarity (concentration). If it rises, thirst
mechanism is triggered
• Pituitary regulation- posterior pituitary releases
ADH (antidiuretic hormone) in response to
increasing serum osmolarity.Causes renal
tubules to retain H20.
• Thirst is a late sign of water deficit
• Renal regulation:-
Nephron receptors sense decreased pressure
(low osmolarity) and kidney secretes RENIN.
• Renin from kidney undergoes renin
angiotensin aldosterone system (RAAS
• Four major stimuli to thirst:
Five ‘Rs’ of intravenous fluid
IV fluids may need to be given urgently to
restore circulation to vital organs following loss
of intravascular volume due
to bleeding, plasma loss, or excessive external
fluid and electrolyte loss, usually from the
gastrointestinal (GI) tract, or severe internal
losses (e.g. from fluid redistribution in sepsis).
IV fluids are sometimes needed for patients who
simply cannot meet their normal fluid
or electrolyte needs by oral or enteral routes but
who are otherwise well in terms of fluid and
electrolyte balance and handling i.e. they are
essentially euvolaemic, with no significant deficits,
ongoing abnormal losses or redistribution issues.
In some patients, IV fluids are used to treat losses from
intravascular and or other fluid compartments, are not
needed urgently for resuscitation, but are still required to
correct existing water and/or electrolyte deficits or ongoing
external losses. These losses are usually from the GI
or urinary tract, although high insensible losses occur
with fever, and burns patients can lose high volumes of what
is effectively plasma.(e.g. cautious, slow replacement to
reduce risks of pontine demyelinosis)
In addition to external fluid and electrolyte losses, some
hospital patients have marked internal fluid distribution
changes or abnormal fluid handling. This type of problem is
seen particularly in those who are septic, otherwise critically
ill, post-major surgery or those with major cardiac, liver or
renal co-morbidity. Many of these patients
develop oedema from sodium and water excess and some
sequester fluids in the GI tract or thoracic/peritoneal cavities.
If patients are receiving IV fluids for resuscitation, reassess
the patient using the ABCDE approach (Airway, Breathing,
Circulation, Disability, Exposure), monitor their respiratory
rate, pulse, blood pressure and perfusion continuously, and
measure their venous lactate levels and/or arterial pH and
base excess according to guidance on advanced life support
(Resuscitation Council [UK], 2011)
• Fluid therapy is used to maintain homeostasis
when enteral intake is insufficient (eg, when a
patient is “nil by mouth” or has reduced
absorption), and to replace any additional losses.
These losses may occur from the gastrointestinal
tract (due to vomiting, diarrhoea or a fistula) or
the urinary tract (eg, diabetes insipidus), or be
caused by blood loss from trauma or surgery.
• In addition, insensible losses can increase during
fever or after suffering from burns because the
barrier function of the skin is impaired.
Fluids can accumulate into spaces that normally
contain minimal fluid volumes (eg, the peritoneal
or pleural cavities) during surgery, anaesthesia or
as a result of inflammatory conditions (eg,
sepsis).This is known as “third spacing” and is
caused by vasodilation and “leakage” of vascular
epithelial walls. This breakdown of normal
compartment integrity can result in loss of
circulating intravascular volume.
Total parenteral nutrition.
As a vehicle for various i.v medications.
Blood and Products
I V Fluids
Non blood I V
Definition : Crystalloid are electrolyte solutions
with small molecules that can diffuse freely from
intravascular to interstitial fluid compartments.
Crystalloids distributes uniformly in extracellular
only 25% of transfused crystalloids remains in
the intravascular space.
75% diffuses into interstitial space
Hence Crystalloids mainly useful to expand the
• One of the most commonly administered crystalloids .
• Using in vitro red cell lysis experiments , Hamburger
ascertained that 0.9% was the NaCl concentration that
was isotonic with human plasma.
• It was not initially developed with the aim of in vivo
administration, yet has entered widespread clinical use
despite having a Na+ and Cl− concentration far in excess
of that of plasma.
• Infusion of 0.9% NaCl leads to an increase in ECF volume ,
more persistent than balanced crystalloids, dilutional
decrease in hematocrit and albumin, increase in Cl− and
K+ concentrations, and decrease in plasma HCO3−.
•1 N sodium chloride solution = 58 grams per
•0.9% sodium chloride = 9 grams per litre
•Composition : Na 154 mEq/L, Cl 154 mEq/L ,
pH 4-5 - Hence it affects the acid base balance of
• Pharmacological basis :
provide major extracellular electrolytes.
corrects both water and electrolyte deficit.
increase the intravascular volume substantially
It causes more expansion of extracellular volume
because of hypertonicity due to increased Na+
relation to ECF.
• Acid base effect causes hyperchloremic
metabolic acidosis caused by high concentration
of chloride in 0.9% NaCl
STRONG ION DIFFERENCE
• Hyperchloremic metabolic acidosis occurs because 0.9%
saline contains strong cations and strong anions in the same
quantity (SID equal to zero). When the plasma chloride
concentration increases after 0.9% saline infusion, the net
positive charge of plasma (SID) is reduced. Conversely,
compensatory mechanisms designed to maintain the plasma
electro-neutrality are activated, thus increasing the plasma
positive charge (H+
) while decreasing the arterial pH.
Water and salt depletion – diarrhoea, vomiting,
Hypovolemic shock- distributed in extracellular
space expanding the intravascular volume. Ideal
fluid to increase blood pressure.
Preferred in case of brain injury, hypochloraemic
metabolic alkalosis , hyponatraemia.
Initial fluid therapy in DKA.
In patients with hyperkalemia eg: renal failure.
Irrigation – washing of body fluids.
Vehicle for certain drugs.
• Avoid in patients with sodium overload : Eg:
• Dehydration with severe hypokalaemia –
deficit of intracellular potassium – NS
without additional K+ supplementation can
aggravate electrolyte imbalance.
• Large volume may lead to hyperchloremic
• In 1880, Sydney Ringer , a British physician
studied the contraction of isolated frog heart.
• He introduced a solution that contained
calcium and potassium in sodium chloride
solution to promote cardiac contraction and
cell viability. This is known as Ringer`s injection
• In early 1930, an American pediatrician named
Alex Hartmann added sodium lactate to
Ringer`s solution as a buffer to metabolic
• This is known as Hartmann`s solution or
Sodium:131mEq/Lt ; chloride – 111mEq/Lt ;
Potassium – 5mEq/Lt; Calcium – 4mEq/Lt ;
Bicarbonate – 29 mEq/Lt.
•(per 100ml) Sodium lactate 320 mg, NaCl
600mg ,KCl 40mg ,CaCl2 27mg.
•RL contains k+
in concentrations that
appropriate free (ionic) concentrations in plasma.
•Addition of these cations reduces Na+
requirement to maintain electrical neutrality.
Advantage of Ringer’s lactate over normal
saline is lack of significant acid base imbalance
•Presence of calcium in ringer’s lactate binds to
situated anticoagulant of stored blood.
•In critically ill patients with impaired lactate
clearance due to circulatory shock or hepatic
insufficiency, Ringer’s lactate infusion can
increase serum lactate levels.
• Ringer`s lactate is the most physiological fluid as
the electrolyte content is similar to that of
plasma. Larger volumes can be infused without
the risk of electrolyte imbalance .
• Sodium content rapidly expands intravascular
volume effective in treatment of hypovolemia.
• Sodium lactate in RL is metabolized to
bicarbonate in the liver useful in correction of
Indications :Indications :
•Correction in severe hypovolaemia.
•Replacing fluid in post operative patients, burns ,
•Diarrhoea induced hypokalemic metabolic
acidosis and hypovolemia.
•Fluid of choice in diarrhoea induced dehydration
in paediatric patients.
•In DKA , provides glucose free water, correct
metabolic acidosis and supplies potassium
•Maintainance fluid during surgery/paediatrics
•Severe liver disease, severe hypoxia
•Severe CHF - lactic acidosis takes place.
•Vomiting or NGT induced alkalosis.
•Simultaneous infusion of RL and blood.
•Certain drugs – amphotericin, thiopental,
ampicillin, doxycycline should not be mixed with
RL – calcium binds with these drugs and reduces
bioavailability and efficiency.
• D5 water
• Dextrose with 0.9% NS ( DNS ).
• Dextrose with 0.45% NS (D1/2NS )
• 10% dextrose.
• 25% dextrose
EFFECT OF DEXTROSE IN FLUID :
Protein sparing effects
Effect of hyperglycemia
EFFECT OF DEXTROSE IN FLUID
Protein sparing effect :
•Earlier it was used to provide calories in patients
who were Nil by mouth
•50 grams of dextrose provides 170 kcal.
•Hence , infusion of 3 litres of D5W at 125 ml per
hour per day provides 510 kcal per day
•It provides energy and prevents endogenous
•It is no longer used frequently as most patients
with long-term Nil by mouth have enteral tube
feedings or TPN.
Composition : Glucose 50 gms/ltr
Pharmacological Basis :
•Corrects Dehydration And Supplies Energy( 170kcal/L)
•Administered safely at the rate of 0.5gm/kg/hr without
Dextrose is metabolised leaving free water
distributed in all compatments of the body.
A proportion of dextrose load contributes to lactate
5% in healthy subjects
85% in critically ill patients. = not the preferred
• Prevention and treatment of intracellular
• IV administration of various drugs
• Prevention of ketosis in starvation, vomiting,
•Adequate glucose infusion protects liver against toxic
•Correction of hypernatraemia –slow IV- provides free
• Neurosurgical procedures- can cause Cerebral oedema
• Acute ischaemic stroke-
– hyperglycemia aggravates cerebral ischaemic brain damage.
– Dextrose metabolism aggravates tissue acidosis in ischaemic
• Hypovolemic shock
– Poor expansion of intracellular volume.
– Faster rate of infusion causes osmotic diuresis worsens shock
and false impression of the hydration status reduced fluid
• Hyponatremia , water intoxication
• Blood transfusion – haemolysis , clumping seen due to
hypotonicity of the solution.
• Uncontrolled DM / severe hyperglycemia.
DEXTROSE SALINE (DNS)
Composition : 5% dextrose with 0.9% NS NaCl– 154 meq/lt each,
glucose 50 gm/ltr.
Pharmacological basis :
• supply major extracellular electrolytes, energy and fluid to
• Conditions with salt depletion ,hypovolaemia- not the ideal fluid
though. Faster rate of infusion causes osmotic diuresis
worsens shock and false impression of the hydration status
reduced fluid replacement.
• Correction of vomiting or NGT aspiration induced alkalosis and
hypochloremia along with supply of calories.
• Anasarca – cardiac, hepatic or renal cause
• Severe hypovolemic shock – rapid correction
is needed. Faster infusion can cause osmotic
diuresis and worsen the condition.
10% DEXTROSE & 25% DEXTROSE
1 liter of fluid has 100 gms glucose and 250 gms glucose
• It is hypertonic crystalloid fluid.
• Supplies energy and prevents catabolism useful
when faster replacement of glucose is needed.
• Rapid correction of hypoglycaemia .
• In liver disease, if given as first drip, it inhibits
glycogenolysis and gluconeogenesis
• Nutrition to patients on maintainance fluid therapy.
• Treatment of hyperkalemia .
•In patients with dehydration , anuria ,
•Avoided in patients with diabetes unless there
•Rapid infusion of 25D can cause glycosuria .
Hence in the absence of hypoglycemia it should
be infused slowly over 45 - 60 min.
• 6 carbon sugar
• Osmotic diuretic
• Freely filterable at glomerulus
• Limited reabsorption from renal tubules
• Resist metabolism
• Pharmacologically inert
• Not absorbed from GIT
• Doesn’t enter cells
• Clearance from plasma by glomerular filtration
Increases plasma osmolarity
Draws fluid from intracellular to extra cellular spaces
Acute expansion of intravascular fluid volume
Decreases brain bulk ,ICP, increases renal blood flow to
Oxygen radical scavenger
Prevents cellular swelling Reduces renal tubular
•Anuria due to severe renal disease.
•Severe pulmonary congestion or frank pulmonary
•Active intracranial bleeding except during
•Progressive renal damage or dysfunction after
institution of mannitol therapy, including increasing
oliguria and azotemia.
• Available as 1.8%, 3% , 5%, and 7.5%
The hypertonic nature of these solutions draws water out
of the intracellular compartment into the extracellular
– Plasma volume expansion: The hypertonic nature of these
solutions draws water out of the intracellular compartment and
into the extracellular (including plasma) volume and may
therefore achieve plasma volume expansion while minimizing the
volume of fluid administered. However, clinical trials have not
shown any benefits.
•Correction of hypo osmolar hyponatremia –
•Treatment of raised ICT- superior to mannitol.
•7.5% - endothelial injury used as sclerosant
INDICATIONS AND LIMITATIONS
Isolyte G :
Vomiting / NGT induced hypochloremic , hypokalemic
NH4 gets converted to H+ and urea in the liver.
Treatment of metabolic alkalosis.
Limitations : hepatic failure , renal failure , metabolic
Richest source of potassium (35mEq)
correction of hypokalaemia.
LIMITATIONS : Renal failure ,burns, adrenocortical
Maintenance fluid for children.
Excessive water loss or inability to concentrate urine
LIMITATIONS : hyponatremia , renal failure.
Extracellular replacement fluid, additional potassium
Corrects Mg deficiency.
Treatment of diarrhoea and metabolic acidosis.
LIMITATIONS : metabolic alkalosis.
A colloid is defined as a high molecular weight (MW)
substance that largely remains in the intravascular
compartment, thereby generating an oncotic pressure.
Colloids are of two types:
Natural - Human albumin
Plasma protein factor
Fresh frozen plasma
Artificial - Gelatin and dextran solutions,
hydroxyethyl starches (HES).
• HYPO-ALBUMINAEMIA CONDITIONS -
After liver transplantation
In conjuction with crystalloids
Critically ill patients-ICU,pulmonary oedema,
congestive cardiac failure
• Heat treated preparation of human serum albumin available
as 5% solution (50 gm/L) and 25% solution (250 gm/L).
Pharmacologic basis –
5% albumin has a colloid osmotic pressure of 20 mmHg
and expands the plasma volume to the same as the volume
Whereas, 25% albumin solution has a colloid osmotic
pressure of 70 mmHg and expands the plasma volume to
almost 4 to 5 times the volume infused.
• Indications :-
1. Plasma volume expansion
2. Correction of hypoprotenemia
3. In therapeutic plasmapheresis as a plasma expander.
Precautions and Contraindications :-
1. Fast infusion will rapidly increase circulatory volume with
resultant volume overload and pulmonary oedema.
2. Contraindicated in patients with severe anemia and cardiac
3. Dehydrated patients may require additional fluids along with
4. Albumin infusion should not be used for parenteral nutrition.
Rate of administration –
For adults, an initial infusion of 25 gm of albumin is
suggested.( 500 ml of 5% solution or 100 ml of 25% solution).
The suggested rate is 2 ml /min for 5% solution and 1 ml/min
for 25% solution.
• These are glucose polymers produced by bacteria
(leucohostoc) incubated in a sucrose medium.
It is available in two forms-
Dextran 40 ( molecular wt. 40,000)
Dextran 70 ( molecular wt 70,000)
Pharmacologic basis –
Plasma volume expansion- D-40 as 10% solution
produces greater expansion than D-70 as 6% solution.
But, duration of expansion is shorter than D-70.
1. Correction of hypovolemia in conditions such as shock, burns,
haemorrhage or trauma.
2. Prophylaxis of deep vein thrombosis.
3. To improve microcirculation and blood flow in threatened
4. Improvement of thromboembolism.
• Side Effects :-
1. Acute renal failure
2. Hypersensitivity reactions
3. It may interfere with blood grouping and cross matching.
• Contraindications :-
1. Severe oliguria and renal failure.
2. Known hypersensitivity reactions.
3. Severe CHF or circulatory overload.
4. Bleeding disorders such as thrombocytopenia.
5. Severe dehydration
• Administration :-
1. Dextran 40 :- It is given as 10% infusion in 0.9% NaCl or
Adults with shock requires 500ml rapid infusion. In first 24
hours, dose not to exceed 20 ml/kg and subsequently 10
ml/kg/day for 5 days.
2. Regime for thromboembolism:-
Day 1 – 500-1000 ml over 4 to 6 hrs.
Day 2 – 500 ml over 4 to 6 hrs.
Upto 10 days – 500 ml over 4 to 6 hrs on alternate days.
Gelatin Polymers (Haemaccel)
• It is available in 3.5% solution in a 500 ml bottle.
Each litre contains :-
Gelatin polymer 35 gms
Sodium 145 mEq
Chloride 145 mEq
Calcium 12.5 meq
Potassium 5.1 mEq
• Indications –
1. For rapid expansion of intravascular volume.
2. Prophylactic use in major surgeries to reduce total volume of
3. For priming of heart lung machine.
• Advantages –
1. Does not interfere with coagulation , blood grouping.
2. Remains in blood for 4-5 hours and expands the plasma
volume by about 50% of infused volume.
( Hydroxyethyl starch)
• It is a synthetic colloid available as 6% solution in isotonic
Pharmacologic basis –
1. It has a osmolarity of about 30 mm Hg
2. It produces greater plasma volume expansion as
compared to dextran.
3. The expanded volume may last for 24 hours.
1. Fewer antigenic properties as compared to dextran
2. It does not interfere with blood grouping and cross matching.
3. Less expensive.
4. Plasma volume expansion greater than albumin.
5. Effect last for about for 24 hours.
• Disadvantages :-
1. Increase in serum amylase concentration.
2. Decreased oxygen carrying capacity.
• Indications, Contraindications, administration :-
1. Similar to dextran.
Colloid Vs. crystalloid for volume resuscitation in
the critically ill patients
• The safety of colloids was first questioned by a
rudimentary meta analysis performed by
Velanovich in 1989.
• The SAFE (Saline versus Albumin Fluid Evaluation)
trial randomized 7000 critically ill patients
requiring fluid resuscitation to receive iso oncotic
albumin or isotonic crystalloid.
• In this study, there was no overall difference in
outcome according to whether patients received
colloids or crystalloids.
A problem-based approach
• The colloid-crystalloid controversy is fueled by the premise that
one type of fluid is optimal in all cases of hypovolemia.
• This seems unreasonable , since no single resuscitation fluid
will perform optimally in all conditions associated with
– life threatening hypovolemia due to blood loss – blood products /
– Hypovolemia due to dehydration – crystalloid resuscitation
• Tailoring the type of resuscitation fluid to the specific cause
and severity of hypovolemia is a more reasoned approach than
using the same type of fluid for all cases of hypovolemia.
Routine fluid calculation
• Holliday and Segar formula-1957
• 4-2-1 rule derived from 100-50-20 rule
determines hourly rate
Depends upon pts weight
Both are effective in normal weight pts
Importance of pH
1. Normal cellular enzymatic reactions
2. Normal ionic concentrations
3. Change in pH can cause cardiac arrhythmias.
4. Act as a marker of an underlying diseases.
Clinical terminology Criteria
Normal pH 7.4(7.35-7.45)
Acidosis pH < 7.35
Alkalosis pH > 7.45
Normal PaCO2 40 mm of Hg
Respiratory acidosis PaCO2 > 45 mm of Hg
Respiratory alkalosis PaCO2 < 35 mm of Hg
Normal HCO3 24 mEq/L
Metabolic acidosis HCO3 < 22 mEq/L
Metabolic alkalosis HCO3 > 26 mEq/L
Regulation of Acid-Base Balance
1. Buffers - These are the chemical systems which maintain the
acid base balance in the body. Eg:bicarbonate,
phosphate, proteins and haemoglobin.
2. Respiratory regulation :- by excretion of volatile acids and
maintaining PaCO2 at optimum concentrations , it has a
double buffering system.
3. Renal regulation :- It acts by balancing the excretion of
hydrogen ions and net reabsorption and production of
Primary Acid-Base Disorders
If initial disturbance affects HCO3,
1. Metabolic Acidosis ( fall in bicarbonate).
2. Metabolic Alkalosis ( rise in bicarbonate).
If initial disturbance affects PaCO2,
1. Respiratory Acidosis (rise in PaCO2).
2. Respiratory Alkalosis (fall in PaCO2).
Compensation in Acid-Base disorders :-
The body’s response to neutralize the effect of the initial insult
on pH homeostasis is called as compensation.
o To maintain normal pH, primary metabolic disorders leads to
compensatory respiratory responses.
o Same direction rule :-
In each case, the compensatory changes are in the same
direction as the primary change.
This is known as Same direction rule.
Disorder Expected compensation
Metabolic Acidosis ( Fall in HCO3) Fall in PaCO2 = 1.5 × HCO3 + 8
Metabolic Alkalosis(Rise in HCO3) Rise in PaCO2 = 0.5 × Rise in HCO3
Respiratory Acidosis Rise in PaCO2
Acute:Rise in HCO3 = 0.1 × Rise in PaCO2
Fall in pH 0.01 × Rise in PaCO2
Chronic: Rise in HCO3 = 0.4 × Rise in PaCO2
Fall in pH = 0.003 × Rise in PaCO2
Respiratory Alkalosis Fall in PaCO2
Acute : Fall in HCO3 = 0.2 × Fall in PaCO2
Rise in pH = 0.01 × Fall in PaCO2
Chronic : Fall in HCO3 = 0.4 × Fall in PaCO2
Rise in pH = 0.002 × Fall in PaCO2
• It is characterized by fall in plasma HCO3 and fall in pH
• Etiology :-
(A) Normal Anion gap - (B) Increased Anion gap –
- Loss of HCO3 : - Metabolic disorders :
diarrhea, proximal RTA lactic acidosis, DKA
- Failure to excrete H+ : - Addition of acids :
distal RTA Salicylate poisoning
- Addition of H+ - Renal failure
• It is subdivided into two types –
A. Specific management of underlying disorder :-
Firstly, underlying disorder should be treated meticulously,
and is the only required treatment in most of the cases.
B. Alkali therapy :–
Bicarbonate administration should be reserved for selective
patients with severe acidosis.
Treatment of all acidotic patients is not only unnecessary but
can also be detrimental.
7.5% sodium bicarbonate 25ml ampoule each ampoule
contains 22.5 mEq sodium and 22.5mEq bicarbonate.
Treatment of metabolic acidosis
Cardiopulmonary resuscitation and shock.
Treatment of hyperkalemia.
Alkaline forced diuresis along with diuretics in treatment
of barbiturates and salicylates.
When to use?
Mild to moderate acidosis can be treated with Ringer’s
lactate or Isolyte E in addition to treatment of underlying
Severe metabolic acidosis can be treated with
How much to give?
Amount of NaHCO3 = 0.6 × Weight × (Desired
HCO3 – Actual HCO3).
• How to infuse?
50% of the deficit is corrected in 4 hours and the rest
over 24 hours.
To avoid irritation of vein and sudden sodium loading , it is
added to D5% and infused at desired rate for correction.
Special Precautions :-
It should not be given as bolus except in emergency cases.
As it is very irritant, establish a proper large i.v line for
Never treat acidosis without treating the etiology.
Avoid in cases of renal failure as it can lead to pulmonary
oedema and tetany.
Never correct acidosis without treating the associated
Do not mix with calcium in the same syringe as it can lead to
calcium carbonate crystals.
Post treatment metabolic alkalosis.
Respiratory alkalosis, metabolic alkalosis and hypokalemia.
Cautious use in congestive heart failure, chronic renal failure,
cirrhosis of liver or hypertension.
• It is characterized by increase in serum HCO3 levels , high pH
and compensatory increase in PaCO2 due to alveolar
1. Generation of metabolic alkalosis – loss of hydrogen ions,
addition of alkali and disproportionate loss of chloride.
2. Maintenance of metabolic alkalosis – volume/chloride
depletion, hypokalemia and aldosterone excess.
1. CNS symptoms :- Neuromuscular
irritability, paresthesia, headache and
2. CVS symptoms :-
Hypotension and arrhythmias.
3. Respiratory symptoms – Hypoxia due to
compensatory mechanism in patients with
pre-existing lung diseases.
4. Others – Weakness, muscle cramps,
1. Correction of volume deficit with isotonic saline along with
potassium and chloride supplementation.
2. Treatment with H2 inhibitors which reduces H+ ions
secretion and further minimizes H+ loss.
3. Discontinue exogenous source of alkali such as NaHCO3 ,
Ringer’s lactate etc.
4. Dilute HCl can be given I.V to lower HCO3 concentration, can
be corrosive and produce thrombophlebitis.
• Saline resistant metabolic alkalosis :-
It requires specific treatment of the underlying etiology-
Surgical treatment of pituitary tumour or adrenal adenoma in
Supportive treatment such as spironolactone, correction of
hypokalemia and sodium restriction.
• It is a clinical disorder characterized by an elevation in the
PaCO2 leading to decrease in pH and compensatory increase
in plasma HCO3.
• Acute Hypercapnia:–
• Anxiety, headache,
• hallucination and coma.
• Chronic Hypercapnia:– Sleep
disturbances, loss of memory,
daytime somnolence, personality
changes and tremors.
• Fall in CSF pH is greater in respiratory
acidosis than in metabolic acidosis.
• CVS manifestations,vasculature.
General Measures :-
1. Treat the underlying cause promptly.
2. Establish patent airway and restore adequate
3. In patient with chronic hypercapnia, search for
aggravating factors, vigorous treatment of
pulmonary infection, bronchodilator therapy can be
• In Acute Respiratory Acidosis:
Major threat is hypoxia and not hypercapnia or
acidosis,so oxygen supplementation is required.
• In Chronic Hypercapnia :
Oxygen therapy be instituted cautiously and in lowest
Since hyoxemia may be the primary and only stimulus
Mechanical Ventilatory Support :
Unstable, symptomatic or progressively hypercapnic patients.
Patients exhibiting signs of muscle fatigue.
Refractory severe hypoxia or apnea.
Depression of respiratory centre.
• Alkali Therapy :-
Avoid alkali therapy except in patients with –
A) Associated metabolic acidosis.
B) Severe acidaemia
C) Severe bronchospasm.
• When hyperventilation reduces the PaCO2 and leads to
• Etiology :-
Pulmonary Diseases – pneumonia,
interstitial fibrosis, edema, emboli.
CHF, hypotension or severe anaemia.
High altitude residence.
Stimulation of Respiratory centre
Psychogenic or voluntary , pain , pregnancy
Rapid correction of metabolic acidosis
It varies with the severity, rate of
onset and underlying disorders.
1.It may be the only sign of the
underlying sepsis or hepatic failure.
2.Common features are light
headache, tingling of the
extremities, circumoral paresthesia
and cardiac arrhythmias.
3.PaCO2 below 20 mm of Hg carries a
grave prognostic sign.
1. Vigorous treatment of the underlying cause.
2. Oxygen supplementation , as hypoxia is a common cause of
3. In absence of hypoxia, patient needs reassurance and
rebreathing in a paper bag.
4. Pre-treatment with acetazolamide minimizes symptoms due
to hyperventilation at high altitudes.
• Sodium is the major ECF cation (sodium value 140 mEq/l.
• Total body sodium is about 5,000 mEq in a normal adult
• 85-90% of sodium is present in ECF and it is responsible for
more than 90% of total osmolality of extracellular fluids.
• Major function of sodium is to maintain ECF volume and
therefore maintain blood pressure.
• ECF volume is the reflection of total body sodium content.
• Daily requirement of sodium is about 100mEq or 6gm of
• It is defined as a plasma conc. of less than 135mEq/L.
• Etiology –
I. Pseudo hyponatremia -
A. Normal osmolality – Hyperlipidemia,
B. High osmolality - Hyperglycemia, Mannitol.
Hyponatremia can be further subclassified
according to effective osmolality, as follows:
Mild Moderate Severe
Anorexia Personality changes Drowsiness
Headache Muscle cramps Diminished reflexes
Nausea Muscular weakness Convulsions
Vomiting Confusion Coma
Lethargy Ataxia Death
• Treatment :-
I. To raise the plasma sodium at a safe rate.
II. To replace sodium or potassium deficit or both.
III.To correct underlying etiology.
Specific treatment :-
1. Removal of specific drugs.eg- diuretics, cyclophosohomide.
2. Management of physical stress, post- operative pain.
3. Specific treatment for adrenal insufficiency, hypothyroidism
• Chronic asymptomatic hyponatremia :-
The targeted rate of plasma sodium correction should not be
greater than 0.5 to 1 mEq/L/hour.
A targeted rate of correction should not exceed 8 mEq/L/day.
A rate of correction higher than the above mentioned can
cause central pontine myelinosis.
• Acute hyponatremia with neurological symptoms :-
Initial rate of correction for plasma sodium should be 1.5-2
mEq/L/hour for the first 3-4 hours or until the neurological
The initial correction should not exceed 10-12 mEq in first 24
Patient may also require anticonvulsant therapy and
• Change in serum sodium concentration for a given infusate :-
Sodium defecit(mEq)=total body weight x (140-ser.sodium)
• It is defined as the plasma concentration of sodium more
than 145 mEq/L .
• Hypernatremia ([Na] > 145 mEq/L) is less common than
hyponatremia, but may affect up to 10% of critically ill
• If severe ([Na] > 160 mEq/L), a 75% mortality may occur
depending on the severity of the underlying disease process.
Clinical features :-
These are primarily neurological, this is state in which dry
sticky mucous membrane is characteristic and also elevated
body temperature is present.
altered mental status
focal neurological deficit
Coma or seizures
• Treatment :-
1. To diagnose and treat specific etiology
2. Correct the fluid deficit = plasma Na – 140 × TBW(kg)×0.6
3.Rate of correction – acute: 1 mEq/L/hr, chronic : 1 mEq/L/2
4.Deterioration of neurological symptoms(cerebral edema).
5. Usually used fluids are isotonic saline, 0.45% saline and 5%
• It is the major intracellular cation present in the body.
• Total body potassium is about 3500 mEq.
• Serum potassium concentration is about 3.5 to 5 mEq/L.
• Intracellular concentration is about 150 mEq/L.
• Normal requirement of potassium is about 50-80 mEq/day.
• It plays an important role in the normal cellular functions and
• This is defined as persistent decrease of the serum potassium
levels below 3.5 mEq/L.
• Responsible for regulation of electrical action potential across
cell membrane specially in cardiac tissues,cellular
1.Poor intake – low dietary intake or potassium
free I.V fluids,refeeding syndrome
2.Intracellular k+ shift-
3.K+ loss-amphotericinB,loop and thiazide
4.Non renal loss – vomiting, diarrhea, large
5.Renal loss – Diuretics, mineralocorticoid
excess, Cushing’s syndrome, magnesium
• It is mainly neuromuscular and cardiac in origin
1. Fatigue, myalgia and muscular weakness are the common
2. Smooth muscle involvement results in constipation, ileus and
3. Hyporeflexia, hypoventilation and virtually complete
4. Increased risk of arrhythmia in patients on chronic digitalis
5. Hepatic encephalopathy in patients with hepatic failure.
Diagnosis of etiology of hypokalemia
2. Urinary potassium excretion –
- Hypokalemia with low renal potassium excretion
- Hypokalemia with high renal potassium excretion :
- metabolic acidosis
- variable pH
- metabolic alkalosis with or without
• In mild to moderate hypokalemia(3-3.4), average dose of
potassium is 60-80 mEq/day along with treatment of
• In severe hypokalemia(<3), more rapid correction is required
and can be done orally. Usual dose is 40-80 mEq/ 6 hourly
under ECG monitoring.
• I.V potassium supplementation is reserved for patients with
severe symptomatic hypokalemia or who cannot ingest oral
Inj. KCl 15% 10 ml ampoule
1 amp = 1.5 gm KCl = 20 mEq.
Pharmacological basis –
Important for neuromuscular regulation
Inability of kidneys to retain potassium
Potassium is lost in certain conditions to maintain conc. Of sodium.
Normal requirement of potassium is 50-60 mEq
Added to various maintenance fluids to counteract
Added to potassium free peritoneal dialysis to maintain
During Cardiac bypass surgery for achieving cardiac standstill
after heart lung bypass.
Basic rules in use of KCl :-
Never give Inj. KCl directly.
Never give more than 40 mEq per litre.
Never infuse more than 10 mEq per hour.
Monitor constantly the levels of potassium and if possible ECG
Cautious use in renal failure.
Never infuse KCl without knowing the potassium status.
• It is the serum potassium levels greater than 5.5 mEq/L is
termed as hyperkalemia.
Although, not as common as hypokalemia , it can lead to
• Etiology :-
1. Increased intake
2. Tissue breakdown
3. Shift of potassium out of cells
4. Impaired excretion
It is essential for bone formation and neuromuscular co-
Contains 1.2 to 1.4 kg of calcium in the body.
Serum calcium – 10 mg/dl.
40% is in ionized form and remaining bound to protein.
Small amount complexed with anions of organic acids.
Regulated by parathormone,Vitamin D and calcitonin.
Clinical features :-
A.Central nervous system – neurologic depression
B.GIT System – constipation
C.Renal system- osmotic diuresis, renal stones
D.CVS – increased heart rate and blood pressure.
A. Measures to increase urinary excretion -
volume expansion and saline diuresis.
B. Measures to inhibit the bone resorption -
C. Measures to decrease intestinal absorption :-
• Decrease in the serum calcium level below 10 mg/dl
2. Post surgical – hungry bone syndrome
3. Defect in vitamin D metabolism –
nutritional , lack of exposure to sunlight
liver diseases, renal failure
vitamin D dependent rickets
4. Miscellaneous –
metabolic or respiratory alkalosis
sepsis, toxic shock syndrome
• Clinical features :-
- Weakness, circumoral and distal extremity paresthesia
- muscle spasm, carpopedal spasm
- mental changes( irritability, depression, psychosis)
- lethargy, confusion , laryngeal spasm
- chvostek’s sign, trousseau’s sign
- chronic hypocalcaemia can lead to calcification of
• Treatment :-
10% calcium gluconate (10 to 20 ml) I.V over 10 minutes is the
usual treatment in emergency conditions.
Severe symptomatic conditions may require infusion of 60 ml
of calcium gluconate in 500 ml of 5% dextrose.
To rule out hypomagnesemia
In long term management of hypocalcaemia, oral elemental
calcium 1 to 3 grams per day is given.
Vitamin D supplementation
• It is critical in bone formation and cellular energy metabolism.
Chiefly intracellular and 1% in ECF.
Serum phosphate level is 3 to 4.5 mg/dl.
Major regulatory factors include parathormone, vitamin D
1. Decreased intestinal phosphate absorption -
vitamin D deficiency
vitamin D dependant rickets
malabsorption, phosphate binding antacids.
2. Increased renal phosphate excretion.
3. Shift of phosphate in intracellular fluid.
• Clinical features :-
I. Muscular abnormalities – proximal muscle weakness,
rhabdomyolysis, impaired diaphragmatic function.
II. Neurological abnormalities – paresthesia, dysarthia,
confusion, seizures and coma.
III.Haematological abnormalities :- Tissue hypoxia, impaired
phagocytosis and opsonization , mineralization defects which
leads to rickets in children and osteomalacia in adults.
• Treatment :-
In cases where , serum phosphate levels are greater than 1
mg/dl, oral phosphate replacement is enough.
Severe hypophosphatemia requires I.V phosphate therapy.
Care should be taken to avoid hyperphosphatemia which can
lead to varied complications.
• It is serum levels greater than 5 mg/dl is defined as
1. Decreased renal excretion
2. Acute tissue destruction
3. Increased renal phosphate reabsorption ( hormonal changes)
4. Miscellaneous -
vitamin D intoxication
Metabolic or respiratory acidosis.
• Clinical features –
1. Neurological manifestations – muscular weakness, loss of
deep tendon reflexes, muscular paresis.
2. Cardiac – hypotension, bradyarrhythmia and cardiac asystole.
3. Hypocalcaemia may result.
• Treatment :-
1. Correction of underlying etiology
2. Restriction of dietary phosphate to 600-900 mg/day.
3. Oral phosphate binders – calcium acetate and calcium
4. Correct hyperphosphatemia before correcting
5. Saline diuresis
Goal=> Hemostasis then restoration of normal circulating
volume and tissue perfusion
Permit hypovolemia to achieve cerebration rather than
normotension, maintain SBP of 70 to 80 mm Hg in
penetrating trauma, or 90 mm Hg in blunt trauma.
Large volumes of IV crystalloids or colloids in early
resuscitation will cause hemodilution and dilute clotting
factors, and saline-based fluids may aggravate the acidosis .
pRBCs, FFP and platelets replaced early.
“High” ratios of FFP to pRBC (e.g., 1:1 to 1:2) are associated
with the best outcomes
Avoidance hyponatremia and hypoosmolality to minimize
cerebral edema in isolated head injuries with a MAP >90
• Rational management => maintain baseline blood volume
and cerebral perfusion avoid decreases in serum Na+,
osmolality, and oncotic pressure.
• Specific management may be required in:
• 1. Increased ICP: Mannitol and hypertonic saline given by
bolus. Hypertonic saline superior to mannitol.
• Restrictive fluid strategies advocated in severe traumatic
• 2.Cerebral vasospasm: “triple-H” therapy
Hypervolemia, Hemodilution, Hypertension
• 3.Intracranial pathologic condition CAUSE cerebral salt
wasting, diabetes insipidus, SIADH. Albumin is => increase
in mortality in traumatic brain injury.
• General measures that should be applied to all
patients, as follows:
– Returning to oral fluids as early as possible
– Ensuring euvolemia to minimize the ADH response
– Not confusing maintenance requirements with the
variable amounts of fluid required because of ongoing
losses (e.g., GI or blood), which should typically be
replaced by isotonic crystalloids, colloids, or blood
– Checking electrolytes at least daily in those still
receiving IV fluids
• Intraoperative – 20-40ml/kg of balanced salt
• Postoperative fluid management should be
reduced to a 2, 1, 0.5 rule; that is,
– 2 mL/kg for the first 10 kg
– 1 mL/kg for the next 10 kg
– 0.5 mL/kg for each kg above 20 kg with an isotonic
• If after 12 hours the child is unable to convert
to oral intake, then a standard hypotonic
solution (D5 0.45% saline) is initiated at the 4-
2-1 rule rate to avoid hypernatremia.
Miller’s Anaesthesia (8th
edition ) – Ronald Miller.
Practical guidelines on Fluid Therapy(2nd
edition) –Dr. Sanjay
Textbook of Physiology – Guyton and Hall.
Textbook of General Surgery – Bailey and Love.
SHAILA SHODHAN KAMAT-IV FLUIDS IN SURGICAL PATIENTS.
WARD PROCEDURES-PATEL AND UPADHYAY