Fluid balance and fluids

management.
Electrolyte abnormalities.
Acid Base abnormalities
Fluid balance
Accurate replacement of fluid deficits necessitates an understanding of
the expected distribution spaces of water, sodium and colloid.
. The sum of intracellular volume (ICV), which constitutes 40% of total
body weight, and extracellular volume (ECV), which constitutes 20% of
body weight, comprises total body water (TBW), which therefore
approximates 60% of total body weight. Plasma volume, equals about
one-fifth of ECV, the remainder of which is interstitial fluid volume (IFV).
Red cell volume, approximately 2L, is part of ICV.
The distribution volume of sodium-free water is TBW. The distribution
volume of infused sodium is ECV, which contains equal sodium
concentrations ([Na+]) in the plasma volume and interstitial fluid. Plasma
[Na+] is approximately 140 mEq/L. The predominant intracellular cation,
potassium, has an intracellular concentration ([K+]) approximately 150
mEq/L. Albumin, the most important oncotically active constituent of ECV,
is unequally distributed in plasma volume (~ 40g/L) and IFV (~ 10g/L). The
IFV concentration of albumin varies greatly among tissues; however, ECV is
the distribution volume for colloid solutions.
TBW content is regulated by the intake and output of water. Water intake
includes ingested liquids plus an average of 750 ml ingested in solid food
and 350 ml that is generated metabolically. Insensible losses are normally 1
L/day and gastrointestinal losses are 100 to 150 mL/day. Thirst, the primary
mechanism of controlling water intake, is triggered by an increase in body
fluid tonicity or by a decrease in ECV.
Reabsorption of filtered water and sodium is enhanced by changes
mediated by the hormonal factors antidiuretic hormone (ADH),
atrial natriuretic peptide (ANP) and aldosterone.
Two powerful hormonal systems regulate total body sodium. The
natriuretic peptides, ANP, brain natriuretic peptide, and C-type
natriuretic peptide, defend against sodium overload and the renin-
angiotensin-aldosterone axis defends against sodium depletion and
hypovolemia.
Aldosterone is the final common pathway in a complex response to
decreased effective arterial volume, whether decrease effective
arterial volume is true or relative, as in edematous states or
hypoalbuminemia
Osmotically active particles attract water across semipermeable
membranes until equilibrium is attained.
The osmolarity of solution refers to the number of osmotically
active particles per liter of solvent; the osmolality, a measurement
of the number of osmotically active particles per kilogram, can be
estimated as follows:

Where osmolality is expressed in mmol/kg, [Na+] is expressed in

mEq/L, serum glucose is expressed in mg/dL, and BUN is blood urea
nitrogen expressed in mg/dL.
A hyperosmolar state occurs whenever the concentration of osmotically
active particles is high. Both uremia (increased BUN) and hypernatriemia
(increased serum sodium) increase serum osmolality. However, because
urea distributes throughout TBW, an increase in BUN does not cause
hypertonicity.
Sodium, largely restricted in ECV, causes hypertonicity, that is,
osmotically mediated redistribution of water from ICV to ECV.
The term tonicity is also used colloquially to compare the osmotic
pressure of a parenteral solution to that of plasma.
Although only a small proportion of the osmotically active particles in
blood consist of plasma proteins, those particles are essential in
determining the equilibrium of fluid between the interstitial and plasma
compartments of ECV.
Fluids management
Fluids are divided into crystalloids and colloids.
Crystalloids are low molecular weight, aqueous solutions with or without glucose. They
equilibrate with all body fluids.
Colloids are of high molecular weight and maintain plasma oncotic pressure and remain
intravascular for some hours.
Water loss is replaced with hypotonic maintenance solutions like 5% Glucose solution.
Water and electrolyte deficits are replaced with isotonic solutions viz., replacement type
fluids like Ringer lactate solution.
Colloids are used to maintain colloidal osmotic pressure, their half life is 3-6 hours.
Indications for colloids are:
Haemorrhagic shock awaiting blood
Fluid resuscitation in severe hypoalbuminaemia or protein losses (burns).
Crystalloids: Colloids:

Ringer lactate Dextrans

Normal saline Gelatins
Darrow’s solution
Hydroxyethyl starch
Glucose solutions
Albumin
Blood
Crystalloids
Ringer lactate (Hartman solution) is isotonic solution (osmolarity 280 mosm/l).
Contains 131 mEq/l Na+, 5 mEq/l K+, 112 mEq/l Cl-, 2 mEq/l Ca2+ and 29 mEq/l
bicarbonate as lactate. Ringer lactate is a crystalloid of choice for blood loss replacement.
Blood should not be given through the same drip set (because Ringer lactate contains
calcium).
Normal saline – it is 0.9% NaCl isotonic solution. Contains 154 mEq/l Na + and 154 mEq/l
Cl-. It is preferred over Ringer lactate for treating hypochloremic metabolic alkalosis,
hyponatremia and brain injury (Ca2+ in lactate can increase the neuronal injury).
Darrow’s solution is 2.5% dextrose, 65 mEq/l Na + and 36 mEq/l K+. It is used to replace
liquid losses from diarrhea.
Glucose solutions are isotonic solutions but with the metabolism of glucose inside the
body become hypotonic.
Colloids
Dextrans (Lomodex) are polysaccharides. Dextrans are used as a plasma expanders. A solution of
smaller molecular weight (30 000 Daltons) is used to improve tissue perfusion by opening up the
microcirculation. These are dextrose starches, the may inhibit anti-platelet effects, antigenicity
and cause anaphylactic reaction. Large molecular weight Dextrans can blocks renal tubules.
Dextrans can interfere with blood grouping and cross matching (because they can cause red cell
aggregation).
Gelatins (Haemaccel) are plasma expander too. They expand plasma effectively for 2 hours (25%
may present in blood after 12 hours). They do not interfere with blood grouping, platelet function
and do not produce severe anaphylactic reactions. Because of these reasons these solutions are in
common use now-a-days. As they contains calcium therefore citrated blood should not be mixed.
Hydroxyethyl starch (HAES-steril) is available as 6% and 10% solution. They have prolonged half
life and expand plasma effectively for hours. These solutions improve microcirculation and hence
improves oxygen delivery in tissues.
Blood is the most useful and life-saving human spare part. It is usually
transfused as replacement when lost. Before administration it is
mandatory to check that the bottle has been previously grouped and
cross-matched for the patient.
Plasma is useful as plasma expander. Reconstituted dried plasma from a
pool of several donors is used. Plasma requires cross-matching.
Albumin (5% and 20%) are used to increase plasma proteins and osmotic
pressure, these are less hazardous than plasma. No cross-matching is
required. Hypersensitivity may be seen in some cases.
The aim of administrating fluid and electrolytes to a patient by
intravenous infusion is to maintain water and electrolyte content at
optimal levels when intake is less or losses excessive. A patient can
withstand deprivation of calories and proteins for weeks but cannot
withstand dehydration for more than 5-6 days.
All metabolic processes of the cell take place in an aqueous phase, the
maintenance of the volume and content of intracellular water is of great
importance. The extracellular fluid has an important role in transport of
nutrients into cells and metabolites out, to be carried to the lungs, liver
and kidney for disposal.
Balanced salt solutions or isotonic are fluids of choice. For pediatric
isolyte solutions with less dextrose are available
Loss in a 60 kg adult:
Urine – 1000 ml
Lungs – 400 ml
Skin – 900 ml, more in hot weather
Stools – 200 ml, more in diarrhea
Total loss of water/day – 2500 ml
Excess fluid losses may occur through:
Exudations and evaporation in burns
Gastrointestinal tract – vomiting, nasogastric suction, intestinal fistulae and diarrhea
Kidney
Haemorrhage
Third space loss due to sequestration following trauma and surgery.

Adequacy of fluid and acid base balance is assessed by the following parameters:
 Heart rate, blood pressure, CVP
 Urinary output
 Serial haematocrit, electrolytes, osmolarity, arterial blood gases.
Fluids for certain clinical situations commonly encountered
Renal failure: Colloids preffered (start with 30% of requirement and
further transfuse fluids as per central venous pressure).
Liver failure: Albumin is preferred.
Intestinal obstruction: Ringer lactate.
ARDS: Initially crystalloids (colloids can be given only after 48 hours).
Burns: For first 24 hours Ringer lactate at a rate of 4ml/kg/% of burns (of
this total fluid 50% is to be given in 8 hours and remaining 50% in next 16
hours). For second day colloids (especially Albumin) are added.
Electrolytes
Sodium (Na+) – normal level 135 – 145 mEq/L

 Sodium, the principal extracellular cation and solute, is essential for generation of
action potentials in neurologic and cardiac tissues.
 Disorders of total body sodium are associated with corresponding increases or
decreases of ECV and plasma volume. Disorders of sodium concentration, that is,
hyponatremia and hypernatremia, usually result from relative excesses or deficits,
respectively, of water.
 Regulation of total body sodium and [Na+] is accomplished primarily by the
endocrine and renal systems. Secretion of aldosterone and ANP control total body
sodium. ADH, which is secreted in response to increased osmolality or decreased
blood pressure, primarily regulates [Na+]. Therefore primary hyperaldosteronism is
associated with hypervolemia and with hypertension, but not with abnormal [Na +].
Hyponatremia ([Na+] under 135 mEq/L)
Hyponatremia may occur in the presence of hypotonicity, normal tonicity,
or hypertonicity; thus it is important to measure serum osmolality to
determine the cause of hyponatremia.
Assessment of volume status is also important in determining the cause.
An excess of total body water is more common than a loss of sodium in
excess of water.
Total sodium content Causes Treatment (always treat the
underlying disorder)

Decreased Diuretics (including osmotic

diuretics); Restore fluid and sodium deficits
Renal tubular acidosis; with isotonic saline
Hypoaldosteronism;
Slat-wasting nephropathies;
Vomiting;
Diarrhea

Normal SIADH (Syndrome of inappropriate

antidiuretic hormone); Water restriction
Hypothyroidism;
Cortisol deficiency

Increased Congestive heart failure; Water restriction

Cirrhosis; Loop diuretics
Nephrotic syndrome
The rate at which hyponatremia develops and the presence of symptoms
determine the aggressiveness of treatment. If hyponatremia has
developed quickly, the patient may develop nausea, vomiting, visual
disturbances, muscle cramps, weakness, hypertension, bradycardia,
confusion, apprehension, agitation, obtundation, or seizures; usually the
sodium content is found to be less than 125 mEq/L. The aggressiveness of
treatment depends on the extent of symptoms.
In the simplest cases fluid restriction may be sufficient. Administration of
loop diuretics may also be indicated. Severe neurologic symptoms require
careful administration of hypertonic (3%) saline. The dose of 3% saline
(513mEq Na+/L) is determined as follows:

Dose mEq/l =
Correction should occur slowly, with serial sodium concentrations
measured.
Below 125 mEq/L, correct at a rate of about 1 mEq/L/hr.
Once a concentration of 125 mEq/L has been achieved, the likelihood of
continued severe neurologic symptoms has diminished. It should be
noted that aggressive correction may result in central pontine
myelinolysis.
Seizures require securing a protected airway, oxygenation, ventilation,
and perhaps administration of anticonvulsants, although seizures are
usually self-limited.
Hypernatremia ([Na+] over 150 mEq/L)
Hypernatremia is less common than hyponatremia and is always
associated with hypertonicity.
Hypernatremia can be associated with either low, normal, or high total
body sodium content. Frequently hypernatremia is the result of decreased
access to free water, as in elderly or debilitated patients with impaired
thirst and decreased oral intake.
Other causes include a lack of antidiuretic hormone (diabetes insipidus)
and an excess sodium intake (either parenterally or intravenously such as
with administration of sodium bicarbonate or 3% sodium chloride).
Most often hypernatremia is associated with fluid deficits, and the
hypovolemia poses the greater challenge to the anesthesiologist.
Complicating this, fluid deficits must be corrected slowly lest cellular
edema ensue. Generally elective surgery should be delayed if serum
sodium levels exceed 150 mEq/L. Hypernatremia increases minimal
alveolar concentration.
Hypernatremia produces neurologic symptoms (including stupor, coma,
and seizures), hypovolemia, renal insufficiency (occasionally progressing
to renal failure), and decrease urinary concentrating ability. Because
hypernatremia frequently results from diabetes insipidus or osmotically
induced losses of sodium and water, many patients are hypovolemic or
bear the stigmata of renal disease.
Total sodium content Causes Treatment (always treat
the underlying disorder)

Decreased Osmotic diuresis; First restore intravascular

Increased insensible losses volume with isotonic fluids;
then correct Na+ with
hypotonic fluids

Normal Diabetes insipidus

(neurogenic, nephrogenic); Correct water loss with
Diuretics; hypotonic fluids
Renal failure

Increased Excessive Na+ Slowly correct fluid deficits;

administration (NaHCO3); Loop diuretics
3% NaCl);
Hyperaldosteronism
Potassium (K+) – normal level – 3.5-5.0 mEq/L

Potassium plays an important role in cell membrane physiology,

especially in maintaining resting membrane potentials and in generating
action potentials in the CNS and heart.
Potassium is actively transported into cell by a Na/K ATPase pump, which
maintains an intracellular [K+] that is at least 30-fold greater than
extracellular [K+]. Intracellular [K+] is normally 150 mEq/L while the
extracellular [K+] is only 3.5 to 5 mEq/L.
The two most important regulators of potassium excretion are plasma
[K+] and aldosterone.
Hypokalemia ([K+] under 3.5 mEq/L)
Hypokalemia may be the result of total body loss of potassium
(gastrointestinal and renal), transcellular shifts in potassium, or
inadequate intake.
Diuretics frequently cause hypokalemia, as do gastrointestinal losses and
renal tubular acidosis. Β-adrenergic agonists, insulin, and alkalosis
(respiratory and metabolic) shift potassium to the intracellular space.
Hypokalemia is not uncommon in pregnant women receiving tocolytic
therapy or in patients requiring inotropic support because β-agonists are
used in both instances.
Hypokalemia produces electrocardiogram abnormalities (ST segment and
T wave depression and onset of U waves) and cardiac arrhythmias (often
premature ventricular contractions and atrial fibrillation).
It also impairs cardiac contractility. These cardiac abnormalities are
usually not seen until serum [K+] decreases to 3 mEq/L.
Hypokalemia is especially worrisome in patients taking digitalis or with
ischemic heart disease or preexisting arrhythmias.
Hypokalemia causes muscle weakness and, when severe, may even cause
paralysis.
Patients with hypokalemia are sensitive to muscle relaxants. But no
definitive data suggest that patients having surgery with potassium levels
as low as 2.6 mEq/L have adverse outcomes.
Treatment: Potassium should be administered at a rate no greater than 0.5
to 1 mEq/L. As a safety measure, no more than 20 mEq of potassium,
diluted in a carrier and run through a controlled infusion pump, should
be connected into a patient’s intravenous lines at any one time.
Hyperkalemia ([K+] over 5 mEq/L)
Hyperkalemia may be either acute or chronic in etiology and secondary to
increased intake, decreased excretion, or intracellular shifts related to
acid-base status. Hyperkalemia may be iatrogenic (e.g., potassium
supplementation, potassium-containing medications) and associated
with massive transfusion, metabolic and respiratory acidosis, and renal
failure (acute and chronic); it may also occur after massive tissue trauma
or rhabdomyolysis.
Medications that may cause hyperkalemia include angiotensin
antagonists and receptor blockers, potassium-sparing diuretics
(spironolactone and triamterene), and succinylcholine.
Hyperkalemia may produce profound weakness. Cardiac conduction
manifestations include enhanced automaticity and repolarization. T waves
become peaked, and there is PR interval and QRS prolongation and an
increased risk for severe ventricular arrhythmias.
Hyperkalemia >6 mEq/L should be corrected before elective procedures.
Usually dialysis is the treatment. Always consider hyperkalemia when a
patient with renal failure suffers cardiac arrest.
Treatment: Emergent treatment of hyperkalemia is threefold. Treat
cardiotoxicity with intravenous calcium chloride. Potassium can be quickly
shifted intracellularly by hyperventilation, β-adrenergic stimulation (e.g., β-
agonist nebulizer), sodium bicarbonate, and insulin (if insulin is given, one
should consider glucose supplementation). Bodily excretion of potassium is
more time-consuming but is accomplished using diuretics and dialysis.
Acid base disturbances may be respiratory or metabolic based on arterial
pH, partial pressure of CO2 (pCO2) and bicarbonate levels (HCO3-)

Blood gas sample: arterial sample is taken either from radial artery or
femoral artery (radial preferred). Sample must be taken in heparinized
syringe (glass syringe preferred over plastic), all air (even minute droplet)
should be removed from syringe and sample to be sent in ice.
Interpretation of normal blood gas analysis
pH: 7.35 to 7.45
pCO2: 35 to 45 mm Hg
HCO3-: 24 to 26 mEq/l
Base deficit: -2 to +2
SpO2 (oxygen saturation): 96 to 98%
(A-a)DO2 (alveolar arterial difference): 3 to 5 mm Hg
Interpretation of normal blood gas analysis
The normal pH is maintained by the normal 20:1 ratio of bicarbonate to carbon dioxide as
described by Henderson-Hasselbalch equation which is:

So if this ratio is normally maintained at 20:1 the pH may be normal inspite of acid base
imbalances or in other words it can be said that acid base abnormalities have been compensated.
To compensate or maintain normal ratio any increase in pCO2 is associated with increase in
bicarbonate (bicarbonate retention by kidney) and any decrease in pCO2 is associated with
decrease in bicarbonate (excess excretion of bicarbonate by kidneys).
Diagnostic approach for establishing the acid base
abnormality
The acid base disturbances may be:
 Respiratory acidosis
 Respiratory alkalosis
 Metabolic acidosis
 Metabolic alkalosis
The problem in interpretation arises when more than one abnormality coexist at a
time e.g., respiratory acidosis in COPD patients may be associated with metabolic
acidosis due to decreased cardiac output (cor pulmonale) and renal flow seen in
these patients.
These acid base disturbances may be acute (non compensated) or chronic
(compensated).
Interpretation of normal blood gas analysis
The diagnostic approach is: first seen the pH. It may be normal, increased or
decreased. Then seen pCO2 – it may be again normal, increased or decreased.
Now see the bicarbonate level, this may be unchanged, decreased or
increased. Now interpret in the following way:
 pH is decreased (<7.35) → look for pCO2:
 Normal pCO2 → HCO3- is decreased → metabolic acidosis + respiratory acidosis
 Increased pCO2 → increased HCO3 - → respiratory acidosis
 Increased pCO2 → decreased or normal HCO3- → respiratory acidosis +
metabolic acidosis
 Decreased pCO2 → decreased HCO3- → metabolic acidosis
Interpretation of normal blood gas analysis
 pH is increased (>7.45) → look for pCO2:
 Increased pCO2→ increased HCO3- → metabolic alkalosis
 Decreased pCO2 → increased HCO3- → respiratory alkalosis + metabolic
alkalosis
 Decreased pCO2 → decreased HCO3- → respiratory alkalosis
 pH is normal (7.35 – 7.45) → look for pCO2:
 Normal pCO2 → normal HCO3- → no acid base abnormality
 Increased pCO2 → increased HCO3- → respiratory acidosis + metabolic alkalosis
 Decreased pCO2 → decreased HCO3- → chronic metabolic acidosis (due to
renal disease) and chronic metabolic alkalosis (due to pulmonary disease)
Respiratory acidosis
Definition: it is defined as increase in pCO2 sufficient enough to decrease the pH to less than 7.35.
Causes:
 Hypoventilation which may be because of overdosage of drugs and anesthetics.
 Disorders of neuromuscular junction effecting muscle respiration.
 Central depression of CNS.
 Lung diseases like COPD etc.
 Excessive CO2 production like malignant hyperthermia.
 Respiratory acidosis may be associated with metabolic alkalosis if there are decreased body stores of
chloride and potassium.
Treatment:
 Mechanical ventilation if pCO2 is high (>50 mm Hg). Acidosis should be treated slowly.
 Treatment of the cause.
Respiratory alkalosis
Definition: it is defined as decrease in pCO2 sufficient to increase the pH to more than 7.45.
Causes:
 Hyperventilation: this is the usual cause during general anesthesia (with hand ventilation there is always a
tendency to hyperventilate).
 Iatrogenic.
 Pregnancy.
 Salicylate poisoning.
 Hypoxia.
 CNS trauma.
Treatment:
 Adjustment of ventilator setting (decrease the frequency) and increasing the rebreathing (i.e., exhaled gases
containing CO2).
 CO2 inhalation.
 Treat the cause.
Metabolic acidosis
Definition: defined as decrease in pH < 7.35.
Causes:
 Renal failure.
 Circulatory failure (shock) leading to accumulation of lactic acid.
 Hepatic failure.
 Diarrhea with loss of bicarbonate.
 Cyanide poisoning.
Metabolic acidosis
Anion gap: also called unmeasured anion concentration. Normally anion
gap is constituted by sulfates, phosphates, organic acids and plasma
proteins. Anion gap mainly constituted by plasma albumin.
Anion gap = Sodium concentration – (Chloride + bicarbonate
concentration)
Normal anion gap = 8 – 16mM/l (average 12 mM/l)
Metabolic acidosis
Conditions associated with normal anion gap:
 Conditions primarily associated with bicarbonate loss is accompanied by
equivalent rise in chloride and hence a normal anion gap. These conditions
are:
 Diarrhea.
 Enerostomies.
 Renal tubular necrosis, obstructive uropathies, chronic pyelonephritis. In
these conditions kidney primarily loses bicarbonates but chloride is retained.
 Adminitistration of hydrogen or ammonium chloride.
 Carbonic anhydrase inhibitors.
Metabolic acidosis
Conditions associated with increased anion gap:
 Diabetic ketoacidosis.
 Ketoacidosis associated with starvation.
 Lactic acidosis: this is the most common cause of metabolic acidosis in
anesthesia and is due to tissue hypoxia.
 Salicylate poisoning.
 Methanol and ethylene glycol poisoning.
 Renal failure, leading to decreased excretion of acid, phosphates and
sulfates.
Metabolic acidosis
Conditions associated with decreased anion gap:
 Hypoalbuminemia.
 Multiple myeloma.
Metabolic acidosis

Treatment:
 
 Sodium bicarbonate:
 Dose can be calculated by formula:

 Half of the calculated dose is to be given immediately and the remaining dose only after getting the next
blood gas analysis report. Is it mandatory to have adequate ventilation before giving sodium bicarbonate
because sodium bicarbonate produces carbon dioxide on metabolism (1 mEq produces 180 ml of CO2)
and can worsen the acidosis. Another problem with sodium bicarbonate is its high hypertonicity (6 times
more than plasma) which can result in hypernatremia and hyperosmolarity.
 Other buffers:
 Carbicarb (Sodium bicarbonate + sodium carbonate): it is a non CO2 generating alternative to sodium
bicarbonate but clinical studies are lacking.
 THAM: non sodium containing compound.
 Treat the cause.
Metabolic alkalosis
Definition: defined as pH > 7.45
Causes:
 Vomiting.
 Ryles’ tube aspration (loss of HCl).
 Diuretics.
 Hypovolemia.
 Diarrhea with loss of chloride.
 Iatrogenic.
Treatment:
 Treat the cause.
 I.v. infusion of ammonium chloride or 0.1 N hydrochloric acid (not more than 0.2 mEq/kg/h).
Summary of findings of acid base disturbances
Abnormality pH pCO2 HCO3-
Respiratory acidosis
Acute (non compensated) ↓↓ ↑↑↑ ↑
Chronic (compensated) ↓ ↑↑↑ ↑↑
Respiratory alkalosis
Acute (non compensated) ↑↑ ↓↓↓ ↓
Chronic (compensated) ↑ or normal ↓↓↓ ↓↓
Metabolic acidosis
Acute (non compensated) ↓↓↓ ↓ ↓↓↓
Chronic (compensated) ↓ ↓↓ ↓↓↓
Metabolic alkalosis
Acute (non compensated) ↑↑↑ ↑↑ ↑↑↑
Chronic (compensated) ↑↑ ↑↑ ↑↑↑