gives clear description of disorders of electrolyte and acid base balance.

1. DISORDERS OF FLUID
AND ELECTROLYTE
BALANCE
&
DISORDERS OF ACID
BASE BALANCE
MOHAMMEDIDRIS HAMED
(MD)

2.  Overview of body fluid and fluid compartments
 Regulation of fluid and electrolyte balance
 Body fluid changes
 Electrolyte imbalance
 Sodium
 Potassium
 Calcium
 Magnesium
 Phosphorous
 Acid-base balance
 Parenteral solutions
 Fluid management
 Preoperative
 Intraoperative
 Postoperative

3. Overview of body fluid and fluid
compartments
 Fluid and electrolyte management is paramount to
the care of the surgical patient
 Changes in both fluid volume and electrolyte
composition occur preoperatively, intraoperatively,
and postoperatively, as well as in response to trauma
and sepsis
 Knowledge of the compartmentalization of body
fluids forms the basis for understanding pathologic
shifts in these fluid spaces in disease states.
 The pathophysiology of electrolyte disorders is
rooted in basic principles of total body water and its
distribution across fluid compartments

4.  Water constitutes about 50-60% of total body weight in
an adult
 Lean tissue and solid organs have higher water content
than fat and bone
 Young males have more water than the elderly, the
obese, or the females
 Total body fluid is distributed mainly between two
compartments
 Intracellular fluid: 2/3rd of total body water
 Extracellular fluid: 1/3rd of total body water
 Plasma: 25% of ECF
 Interstitial fluid: 75% of ECF
 All compartments arein osmotic equilibrium with each
other

6. The Intracellular Fluid
 Separated from the ECF by a cell membrane
that is highly permeable to water but not to
most of the electrolytes in the body
 Cells contain large amounts of protein, almost
four times as much as in plasma
 Potassium, phosphate, magnesium, and
sulphate are the principal electrolyte
constituents

7. The Extracellular Fluid
 Because the plasma and interstitial fluid are
separated only by a highly permeable capillary
membrane, their ionic composition is similar
 The most important difference between the two
compartments is the higher concentration of
protein in the plasma
 Due to the Donnan effect, the concentration of
cations is slightly greater in the plasma than in the
interstitial fluid
 The principal electrolytes are sodium, chlorine,
and bicarbonate ions

9. Regulation of fluid and electrolyte
balance
 Water is added to the body by two major
sources: ingestion, and oxidation of
carbohydrates
 Fluid is lost as urine, sweat, faeces and by
insensible water loss from the lungs and skin
 The most important means by which the body
maintains a balance between water intake and
output, as well as balance between intake and
output of most electrolytes in the body, is by
controlling the rates at which the kidneys
excrete these substances

10.  Normal adults are considered to have a minimal
obligatory water intake or generation of approximately
1600 mL per day, composed of the following:
 Ingested water – 500 mL
 Water in food – 800 mL
 Water from oxidation – 300 mL
 The sources of obligatory water output in normal
adults are composed of the following:
 Urine – 500 mL
 Skin – 500 mL
 Respiratory tract – 400 mL
 Stool – 200 mL

11. Body fluid changes
 Disorders in fluid balance may be classified
into three general categories: disturbances in
 Volume
 Concentration
 Composition
 Although each of these may occur
simultaneously, each is a separate entity with
unique mechanisms demanding individual
correction.

12. Disturbances in Volume
 Because sodium is the principal extracellular
cation and is restricted to the ECF, adequate body
sodium is necessary for maintenance of
intravascular volume
 The kidney determines sodium balance because
there is little homeostatic control of sodium intake
 It regulates sodium balance by altering the
percentage of filtered sodium that is reabsorbed
along the nephron
 The renin-angiotensin system is an important
regulator of renal sodium excretion and
reabsorption
 Atrial natriuretic peptide is also important in the
case of volume expansion

13.  Volume deficit
 Extracellular volume deficit is the most common fluid
disorder in surgical patients and can be either acute or
chronic.
 Acute volume deficit is associated with cardiovascular
and central nervous system (CNS) signs.
 Chronic volume deficits display tissue signs, such as a
decrease in skin turgor and sunken eyes, in addition to
cardiovascular and CNS signs.
 Most common surgical cause is loss of GI fluids from
nasogastric suction, vomiting, diarrhea, or
enterocutaneous fistula
 In addition sequestration secondary to soft tissue
injuries, burns, and intra-abdominal processes such as

15.  Diagnosis
 careful history will usually determine the etiologic cause of
hypovolemia
 Nonspecific symptoms including fatigue, weakness, thirst, and
postural dizziness and more severe symptoms and signs include
oliguria, cyanosis, abdominal and chest pain, and confusion or
obtundation
 On examination, diminished skin turgor and dry oral mucous
membranes are less than ideal markers of a decreased ECFV in
adult patients; more reliable signs of hypovolemia include a
decreased jugular venous pressure (JVP), orthostatic
tachycardia (an increase of >15–20 beats/min upon standing),
and orthostatic hypotension (a >10–20 mmHg drop in blood
pressure on standing).
 More severe fluid loss leads to hypovolemic shock.
 Routine chemistries may reveal an increase in blood urea
nitrogen (BUN) and creatinine, reflective of a decrease in GFR.

16.  Treatment
 The therapeutic goals in hypovolemia are to
restore normovolemia and replace ongoing fluid
losses.
 Mild hypovolemia can usually be treated with oral
hydration and resumption of a normal
maintenance diet.
 More severe hypovolemia requires intravenous
hydration, tailoring the choice of solution to the
underlying pathophysiology.

17.  Volume overload
 May be iatrogenic or secondary to renal dysfunction, congestive heart failure, or
cirrhosis
 Both plasma and interstitial fluid are usually increased
 Symptoms are primarily pulmonary and cardiovascular
 pathology
 hormonal and circulatory responses to surgery result in postoperative conservation and
retention of sodium & water independent of the status of the ECF volume.
 ADH released during anesthesia and surgical stress, promotes water conservation by the
kidneys.
 Renal vasoconstriction and increased aldosterone activity reduce sodium excretion.
Consequently, if fluid intake is excessive in the immediate postoperative period,
circulatory overload may occur.
 The tendency for water retention may be exaggerated in heart failure, liver disease, renal
disease, or if hypoalbuminemia is present
 Management
 Alleviating the underlying cause
 Restrict Na+ intake when mild
 Restriction of fluid intake
 Diuretics(take care in CHF)

19. Concentration Changes
(Osmolality/Osmolarity)
 Maintenance of a normal osmolality depends on control of water
balance
 The plasma osmolality is tightly controlled between 285 and 295
mOsm/kg through regulation of water intake and urinary losses
 Small increase in plasma osmolality stimulates thirst
 Urinary water losses are regulated by the secretion of
antidiuretic hormone (ADH), which increases in response to an
increasing plasma osmolality
 ADH increases tubular resorption of water
 Control of osmolality is subordinate to maintenance of an
adequate intravascular volume (i.e., the control of effective
intravascular volume always takes precedence over control of
osmolality)
 Changes in serum sodium concentration are inversely
proportional to total body fluid. Therefore, abnormalities in total
body fluid are reflected by abnormalities in serum sodium levels

20. Hyponatremia
 Serum sodium concentrations below 135
meq/L
 Occurs when there is an excess of
extracellular water relative to sodium
 Extracellular volume could be high, normal, or
low
 In most cases, sodium concentration is
decreased as a consequence of either sodium
depletion or dilution

21.  Dilutional hyponatremia frequently results from
excess extracellular water and therefore is
associated with a higher extracellular volume
status. The causes can be:
 Excessive oral water intake or iatrogenic intravenous
excess free water administration
 Increased secretion of ADH, especially postoperative
patients
 Antipsychotic drugs, tricyclic antidepressants, and
ACE inhibitors (esp. in elderly)
 Physical signs of volume overload are often
absent
 Lab evaluation reveals hemodilution

22.  Depletional causes are associated with either
 Decreased sodium intake: E.g. consumption of a
low-sodium diet or use of enteral feeds or,
 Increased loss of sodium containing fluids: E.g.
GI losses from vomiting, diarrhoea, prolonged
nasogastric suctioning, and renal losses due to
diuretic use or primary renal disease
 A concomitant ECF volume deficit is common
 Associated with low urine sodium levels (<20
mEq/L) in the absence of renal sodium
wasting

23.  Hyponatremia can also be seen with an
excess of solute relative to free water, such as
with untreated hyperglycaemia or mannitol
administration
 Water is shifted from ICF to the ECF
 Hence, for every 100mg/dL rise in plasma
glucose above normal, the plasma sodium
should decrease by 1.6 meq/L
 Lastly, extreme elevations in plasma lipids or
proteins can cause pseudohyponatremia

25. Signs and Symptoms
 Depend on the degree of deficit and the rapidity with
which it occurred
 Clinical manifestations primarily have a CNS origin
and are related to cellular intoxication and
associated increase in intracranial pressure
 Muscle cramps and weakness, anorexia, nausea,
emesis, malaise, lethargy, confusion, agitation,
headache, seizure, coma, and decreased reflexes
can be seen
 Patients may develop hypothermia and Cheyne-
Stokes respirations
 Chronic hyponatremia is more tolerated as the brain
cells can decrease their osmolality to decrease the
osmotic gradient

26. Treatment
 Most cases can be treated by free water restriction
and, if severe, sodium administration
 If neurologic symptoms are present, 3% normal
saline should be used to increase the sodium by no
more than 0.5 mEq/L per hour to a maximum
increase of 12 mEq/L per day, and even more slowly
in chronic hyponatremia
 Rapid correction can lead to pontine myelinolysis
(manifested by dysarthria, dysphagia, paraparesis
or quadriparesis, behavioral disturbances, lethargy,
confusion, disorientation, obtundation, seizures and
coma). The neurologic effects are generally
catastrophic and irreversible and may result in

27. Hypernatremia
 Serum sodium concentrations above 145 meq/L
 Results from either a loss of free water or a gain
of sodium in excess of water
 Extracellular volume could be high, normal, or low
 Hypervolemic hypernatremia usually is caused
either by:
 Iatrogenic administration of sodium-containing fluids
(including NaHCO3) or
 Mineralocorticoid excess (E.g. hyperaldosteronism,
Cushing’s syndrome, and CAH)
 Urine sodium concentration is typically >20 mEq/L
an urine osmolarity is >300 mOsm/L

28.  Normovolemic hypernatremia can result from:
 Renal causes (E.g. diabetes insipidus, diuretic use, and renal disease)
 In surgical ICU patients, a frequent cause of hyponatremia is SIADH.
 Nonrenal water loss (E.g. from the GI tract or skin)
 Hypovolemic hypernatremia can occur because of nonrenal causes
secondary to:
 Relatively isotonic GI fluid losses (E.g. diarrhoea) or hypotonic fluid loss from
skin due to fever, loss via tracheotomies during hyperventilation,
thyrotoxicosis, and use of hypertonic glucose solution for peritoneal dialysis
 With nonrenal water loss, the urine sodium concentration is <15 mEq/L
and the urine osmolarity is >400 mOsm/L.
 Transurethral resection syndrome
 rare but potentially life-threatening complication of a transurethral resection of
the prostate procedure
 as a consequence of the absorption into the prosthatic venous sinuses of the
fluids used to irrigate the bladder during the operation
 Symptoms and signs are varied and unpredictable, and result from fluid
overload and disturbed electrolyte balance and hyponatraemia

29. Signs and Symptoms
 Symptoms usually occur in patients with impaired
thirst or restricted access to fluid, because thirst will
result in increased water uptake
 Water shifts from intracellular fluid to the
extracellular space which causes cerebral
dehydration. This can put traction on cerebral
vessels and lead to subarachnoid haemorrhage
 CNS symptoms can range from restlessness and
irritability to seizures, coma, and death
 Tachycardia, orthostasis, and hypotension are
classic for hypovolemic hypernatremia
 Dry, sticky mucous membranes are unique in
hypovolemic hypernatremia

31. Treatment
 Treat associated water deficit
 Volume should be restored with normal saline before
concentration abnormality is addressed
 Water deficit (L) = (serum sodium-140)/140 * total body water
 Water deficit is replaced using hypotonic fluid such as 5%
dextrose, 5% dextrose in ¼ NS, or enterally administer water
 Rate of decrease should not be greater than 1 mEq/h and 12
mEq/d for acute and even slower (0.7 mEq/h) for chronic
hypernatremia for fear of cerebral edema and herniation
 Hypernatremia is less common than hyponatremia but has a
worse prognosis

32. Composition Changes
 The solute composition of the ICF and ECF
compartments differs markedly.
 ECF contains principally sodium, chloride, and
bicarbonate, with other ions in much lower
concentrations.
 ICF contains mainly potassium, organic
phosphate, sulfate.
 Compositional abnormalities of importance
include changes in
 Potasium, calcium and magnesium balance
 acid-base balance

33. Potassium
 Average dietary intake is approximately 50-100
mEq/d, which in the absence of hypokalaemia is
excreted mainly in the urine
 Although only 2% of the total body potassium is
located in the ECF, this small amount is critical for
cardiac and neuromuscular function
 Minor changes can have major effects in cardiac
activity (98% in the ICF)
 Distribution of potassium in the compartments is
influenced by factors such as surgical stress,
injury, acidosis, and tissue catabolism

34.  Hyperkalemia
 Defined as serum potassium concentration above
5.0 mEq/L
 Caused by:
 Excessive potassium intake
 IV supplementation, oral intake, transfusion
 Increased release of potassium from cells
 Haemolysis, rhabdomyolysis, crush injuries, acidosis,
hyperosmolality (E.g. hyperglycemia or IV mannitol)
 Impaired excretion by kidneys
 Potassium-sparing diuretics, ACE inhibitors, NSAIDS,
acute and chronic renal insufficiency

35.  Signs and Symptoms
 Primarily GI, neuromuscular, and cardiovascular
 GI symptoms include nausea, vomiting, intestinal
colic, and diarrhoea
 Neuromuscular symptoms range from weakness to
ascending paralysis to death
 ECG changes include (early) high peaked T waves,
flattened P wave, prolonged PR interval, and (late)
widened QRS complex, sine wave formation and
ventricular fibrillation
 Hemodynamic symptoms of arrhythmia and cardiac
arrest follow

37.  Treatment
 Goals of therapy are to
 reduce total body potassium,
 cation-exchange resin such as Kayexalate that binds
potassium in exchange for sodium (oral/rectal)
 Remove potassium supplementation in IV fluids and
enteral and parenteral solutions
 shift potassium from the ECF to the ICF, and
 Glucose 1 ampule of D50
 regular insulin 5–10 units IV
 Bicarbonate 1 ampule IV
 β -adrenergic agonists like albuterol
 protecting the cells from effects of high potassium
 Calcium gluconate 5–10 mL of 10% solution (immediate if
cardiac ssx are there)
 And when all else fails, dialysis

38.  Hypokalemia
 Serum potassium concentration below 3.5 mEq/L
 Much more common hyperkalemia in the surgical
patient than
 May be caused by inadequate intake or excessive
renal excretion of potassium. E.g. pathologic
secretions of the GI including diarrhoea, vomiting, and
intracellular shift from metabolic alkalosis or
following insulin therapy
 Potassium decreases by 0.3 mEq/L for every 0.1
increase in pH above normal
 Drugs such as amphotericin and aminoglycosides
induce magnesium depletion and cause renal
potassium wastage

39.  Signs and Symptoms
 Failure of normal contractility of GI smooth,
skeletal, and cardiac muscles
 Ileus, constipation, weakness, fatigue, diminished
tendon reflexes, paralysis, and cardiac arrest
 In the setting of ECF depletion, symptoms may be
masked initially and then worsened by further
dilution during volume repletion
 ECG changes include U waves, T-wave flattening,
ST-segment changes, and arrhythmias (with
digitalis therapy)

40.  Treatment
 Potassium replenishment is indicated at a rate
determined by symptoms
 Oral repletion is adequate for mild, asymptomatic
hypokaelemia
 If IV repletion is indicated, use no more than 10
mEq/h in an unmonitored setting
 Under continuous ECG monitoring, 40 mEq/h and
even higher rates are possible
 Caution in oligouria or impaired renal function

41. Calcium
 The vast majority of the body’s calcium is contained within the
bone matrix with <1% in the ECF
 Serum calcium is found in three forms
 Protein found: 40%
 Complexed to phosphate and other anions: 10%
 Ionized: 50% (responsible for neuromuscular stability)
 Unlike changes in albumin, changes in pH will affect the ionized
calcium concentration. Acidosis decreases protein binding,
thereby increasing the ionized fraction of calcium
 Daily calcium intake is 1 to 3 g. Most is excreted via the bowel
 Regulation is under complex hormonal control and
disturbances in metabolism are relatively long term and less
important in the acute surgical setting
 If total serum calcium is measured, the albumin concentration
must be taken into consideration: adjust total serum calcium
down by 0.8 mg/dL for every 1 g/dL decrease in albumin

42.  Hypercalcemia
 Defined as serum calcium level above 8.5-10.5
mEq/L or an increase in ionized calcium level
above 4.8 mg/dL
 Primary hyperparathyroidism (outpatient
setting) and malignancy (hospitalized patient),
from either bony metastasis or secretion of PTH-
related protein account for most cases

43.  Signs and Symptoms
 Vary with degree of severity
 Neurologic impairment, musculoskeletal weakness
and pain, renal dysfunction, and GI symptoms of
nausea, vomiting, and abdominal pain
 Cardiac symptoms can be manifest as hypertension,
cardiac arrhythmias, and a worsening of digitalis
toxicity
 ECG changes in hypercalcemia include shortened QT
interval, prolonged PR and QRS intervals, increased
QRS voltage, T-wave flattening and widening, and
atrioventricular block (which can progress to complete
heart block and cardiac arrest)

44.  Treatment
 Required when symptoms appear (usually at
levels >12mg/dL)
 The critical level for serum calcium is 15 mg/dL,
when the above-mentioned symptoms may
progress to death
 Initial treatment aimed at repleting the
associated volume deficit and then brisk
diuresis with normal saline
 Treat underlying malignancy

45.  Hypocalcemia
 Serum calcium less than 8.5 mEq/L or a decrease in
ionized calcium level below 4.2 mg/dL
 Pancreatitis, massive soft tissue infections such as
necrotizing faciitis, renal failure, pancreatic and small
bowel fistulas, hypoparathyroidism, toxic shock
syndrome, abnormalities in magnesium levels and
tumor lysis syndrome
 Removal of parathyroid adenoma
 Malignancies associated with osteoblastic such as
breast and prostate
 Massive blood transfusion with citrate sequestration

46.  Signs and Symptoms
 Clinical features occur when ionized fraction falls below 2.5
mEq/dL
 paresthesias of the face and extremities, muscle cramps,
carpopedal spasm, stridor, tetany, and seizures
 Patients will demonstrate hyperreflexia and may exhibit
positive Chvostek’s sign (spasm resulting from tapping
over the facial nerve) and Trousseau’s sign (spasm
resulting from pressure applied to the nerves and vessels
of the upper extremity with a blood pressure cuff)
 Hypocalcemia may lead to decreased cardiac contractility
and heart failure. ECG changes of hypocalcemia include
prolonged QT interval, T-wave inversion, heart block, and
ventricular fibrillation

47.  Treatment
 Asymptomatic can be treated with oral or IV
calcium.
 Acute symptomatic should be treated with IV 10%
Calcium gluconate to achieve a serum
concentration of 7 to 9 mg/dL
 Associated deficits in magnesium , potassium,
and Ph must be corrected
 Hypocalcemia will be refractory if coexisting
hypomagnesimia is not corrected first

48. Phosphate
 Is the primary intracellular divalent anion
 Involved in energy production during glycolysis
 Tightly controlled by renal excretion

49.  Hyperphosphatemia
 Due to decreased urinary excretion, increased
intake, or endogenous mobilization of phosphorus
 Most in renal impairment
 Cell destruction leads to its release
 Mostly asymptomatic but prolonged
hyperphosphatemia can lead to metastatic
deposition of soft tissue calcium-phosphate
complexes
 Phosphate binders such as sucralfate or aluminium
containing antiacids can lower the levels
 Calcium acetate for concurrent hypocalcemia
 Dialysis in renal failure

50.  Hypophosphatemia
 Due to decrease in intake, an intracellular shift, or
increased excretion
 Malabsorption or administration of phosphate binders
decreases uptake
 Most acute cases are due to intracellular shifts due to
respiratory alkalosis, insulin therapy, refeeding
syndrome, and hungry bone syndrome
 Clinical symptoms only in significant fall
 Cardiac dysfunction or muscle weakness due to
impaired oxygen availability or decreased high energy
phosphates
 Oral or parenteral repletion as needed

51. MAGNESIUM
 4th most common mineral in the body
 Predominantly an ICF cation
 A third of plasma ion is bound to albumin
 Approximately half is in the bone and slowly
exchangeable
 It should be replaced until levels are at the upper
limit of normal
 Magnesium regulation relies heavily on the kidney

52.  Hypomagnesemia
 Magnesium depletion is a common problem in
hospitalized patients, particularly in the critically ill.
 Depletion is characterized by neuromuscular and CNS
hyperactivity. Symptoms are similar to those of calcium
deficiency, including hyper -active reflexes, muscle
tremors, tetany, and positive Chvostek’s and
Trousseau’s signs
 ECG changes include prolonged QT and PR intervals,
Torsade de pointes (polymorphic ventricular
tachycardia)
 Important because it might produce hypocalcemia and
lead to persistant hypokalemia
 Oral replenishment if mild, otherwise IV replenishment
(with care)
 Simultaneous calcium gluconate can help reduce

54.  Hyermagnesemia
 Rare; can be seen in severe renal insufficiency
and impaired magnesium excretion
 Magnesium containing antiacids and laxatives
 Massive trauma, burns, or severe acidosis
 Nausea, vomiting, neuromuscular dysfunction
with weakness. Lethargy, hyporeflexia, impaired
cardiac conduction leading to hypotension and
arrest (similar ECG findings as hyperkalemia)

55. Acid-Base Balance
 The pH of body fluids is maintained within a narrow range
despite the ability of the kidneys to generate large amounts of
HCO3− and the normal large acid load produced as a by-
product of metabolism.
 This endogenous acid load is efficiently neutralized by buffer
systems and ultimately excreted by the lungs and kidneys.
 Important buffers include intracellular proteins and
phosphates and the extracellular bicarbonate–carbonic acid
system.
 Compensation for acid-base derangements can be by
respiratory mechanisms (for metabolic derangements) or
metabolic mechanisms(for respiratory derangements).
 Unlike the prompt change inventilation that occurs with
metabolic abnormalities, the compensatory response in the
kidneys to respiratory abnormalities is delayed.

56.  Metabolic Acidosis
 Metabolic acidosis results from an increased intake
of acids, an increased generation of acids, or
increased loss of bicarbonate.
 The body responds by several mechanisms,
including:
 producing buffers (extracellular bicarbonate and
intracellular buffers from bone and muscle),
 increasing ventilation (Kussmaul’s respirations), and
 Renal by increasing reabsorption and generation of
bicarbonate and also will increase secretion of hydrogen
and thus increase urinary excretion of NH4
+ (H+ + NH3
+ =
NH +).

57.  Metabolic acidosis with a normal AG results
from exogenous acid administration (HCl or
NH4
+), from loss of bicarbonate due to GI
disorders such as diarrhea and fistulas or
ureterosigmoidostomy, or from renal losses.

58.  Evaluation of a patient with a low serum
bicarbonate level and metabolic acidosis
includes determination of the anion gap (AG),
an index of unmeasured anions.
 Metabolic acidosis with an increased AG occurs
either from ingestion of exogenous acid such as
from ethylene glycol, salicylates, or methanol, or
from increased endogenous acid production
(ketoacidosis, lactic acidosis, renal insufficiency)
 A common cause of severe metabolic acidosis in
surgical patients is lactic acidosis.

59.  Treatment
 Directed to ward correcting the underline
problem. (example; in a patient with circulatory
shock, to restore perfusion with volume
resuscitation rather than giving bicarbonate)
 Bicarbonate given in severe cases

60.  Metabolic Alkalosis
 Metabolic alkalosis results from the loss of fixed acids or the
gain of bicarbonate.
 The majority of patients also will have hypokalemia, because
extracellular potassium ions exchange with intracellular
hydrogen ions and allow the hydrogen ions to buffer excess
HCO3-
 Vomiting with an obstructed pylorus results only in the loss of
gastric fluid, which is high in chloride and hydrogen, and
therefore results in a hypochloremic alkalosis.
 Initially the urinary bicarbonate level is high in compensation
and hydrogen ion reabsorption also ensues
 Treatment includes replacement of the volume deficit with
isotonic saline and then potassium replacement once

61. Respiratory Derangements
 Normally, pCO2 is tightly maintained by
alveolar ventilation, controlled by the
respiratory centers in the pons and medulla
oblongata

62.  Respiratory Acidosis
 Respiratory acidosis is associated with the
retention of CO2 secondary to decreased alveolar
ventilation.

63.  Treatment of acute respiratory acidosis is
directed at the underlying cause and
measures to ensure adequate ventilation are
also initiated.
 In the chronic form of respiratory acidosis, the
partial pressure of arterial CO2 remains
elevated and the bicarbonate concentration
rises slowly as renal compensation occurs to
ensure ,adequate ventilation are also initiated.

64.  Respiratory Alkalosis
 In the surgical patient, most cases of respiratory alkalosis
are acute and secondary to alveolar hyperventilation.
 Causes include pain, anxiety, and neurologic disorders,
including central nervous system injury and assisted
ventilation.
 Drugs such as salicylates, fever, gram-negative bacteremia,
thyrotoxicosis, and hypoxemia are other possibilities.
 Acute hypocapnia can cause an uptake of potassium and
phosphate into cells and increased binding of calcium to
albumin, leading to symptomatic hypokalemia,
hypophosphatemia, and hypocalcemia with subsequent
arrhythmias, paresthesias,muscle cramps, and seizures.
 Treatment should be directed at the underlying cause,
but direct treatment of the hyperventilation using
controlled ventilation may also be required.

65. Parenteral solutions
 Crystalloids
 aqueous solutions of mineral salts or other water-soluble molecules
 E.g., normal saline, Ringer's lactate, 5% dextrose in water, 5% dextrose in
normal saline
 Colloids
 contain larger insoluble molecules, such as gelatin
 A number of commercially available electrolyte solutions are available for
parenteral administration
 The type of fluid administered depends on the patient’s volume status and
the type of the concentration or compositional abnormality present
 Both lactated Ringer’s solution and normal saline are considered isotonic
and are useful in replacing GI losses and correcting extracellular volume
deficits
 The less concentrated sodium solutions such as 0.45% sodium chloride,
are useful for replacement of ongoing GI losses as well as for maintenance
fluid therapy in the postoperative period
 Addition of 5% dextrose supplies 200 kcal/L and is necessary for solutions
containing <0.45% sodium chloride to maintain osmolality and prevent

67.  Alternative Resuscitative fluids
 Hypertonic saline solutions (3.5%, 5%, and 7.5%)
 For correction of severe sodium deficits and to
decrease ICP
 Colloids
 Due to their molecular weight, they are confined to the
intravascular space, and their infusion results in more
efficient transient plasma volume expansion*
 Four major types are available
 Albumin
 Dextrans
 Hetastarch
 Gelatins

69. Preoperative Fluid Therapy
 With the induction of anesthesia, compensatory
mechanisms are lost, and hypotension will develop
if volume deficits are not appropriately corrected
before the time of surgery
 Hemodynamic instability during anesthesia is best
avoided by correcting known fluid losses, replacing
ongoing losses, and providing adequate
maintenance fluid therapy preoperatively
 The administration of maintenance fluids should be
all that is required in an otherwise healthy individual
(presumed with no pre-existing deficit or ongoing
fluid losses and in no need of replenishment) who
may be under orders to receive nothing by mouth
for some period before the time of surgery

70.  The frequently used formula for calculating the
volume of maintenance fluids is:-
 For the first 0–10 kg Give 100 mL/kg per day
 For the next 10–20 kg Give an additional 50
mL/kg/day
 For weight >20 kg Give an additional 20
mL/kg/day

71. Intraoperative Fluid Therapy
 In addition to measured blood loss, major open
abdominal surgeries are associated with
continued extracellular losses in the form of bowel
wall edema, peritoneal fluid, and the wound
edema during surgery
 Large soft tissue wounds, complex fractures with
associated soft tissue injury, and burns are all
associated with additional third-space losses that
must be considered in the operating room
 Although no accurate formula can predict
intraoperative fluid needs, replacement of ECF
during surgery often requires 500 to 1000 mL/h of
a balanced salt solution to support homeostasis

72. Postoperative Fluid Therapy
 Postoperative fluid therapy should be based
on the patient’s current estimated volume
status and projected ongoing fluid losses.
 Any deficits from either preoperative or
intraoperative losses should be corrected, and
ongoing requirements should be included
along with maintenance fluids
 The adequacy of resuscitation should be
guided by the restoration of acceptable values
for vital signs and urine output

73.  References
 F. Charles Brunicardi et al: Schwartz’s Principles
of Surgery, 10th edition, 2015
 Guyton and Hall Textbook of Medical Physiology,
12th edition, 2011
 Review notes from past years