Fluid and Electrolyte Management

of the Surgical Patient

Yonas Ademe
Sep, 2017

1
Body fluids

2
 Total Body Water
• Water constitutes approximately 50% to 60% of total body
weight
– This estimate should be adjusted downward approximately 10%
to 20% for obese individuals and upward by 10% for
malnourished individuals
– The highest percentage of TBW is found in newborns, with
approximately 80% of their total body weight comprised of
water

• The relationship between total body weight and total

body water (TBW) is relatively constant for an individual
and is primarily a reflection of body fat
3
 Composition of Fluid Compartments
• The ECF compartment is balanced between sodium, the
principal cation, and chloride and bicarbonate, the principal
anions

• The intracellular fluid compartment is composed primarily of

the cations potassium and magnesium, and the anions
phosphate and sulfate, and proteins

• The concentration gradient between compartments is

maintained by ATP driven sodium-potassium pumps located
with in the cell membranes

4
 Cont.
• The composition of the plasma and interstitial fluid differs only
slightly in ionic composition
– Plasma has a slightly higher protein content
• These proteins add to the osmolality of the plasma and contribute to the
balance of forces that determine fluid balance across the capillary
endothelium
• Water is distributed evenly throughout all fluid compartments
of the body so that a given volume of water increases the
volume of any one compartment relatively little
– Sodium, however, is confined to the ECF compartment and it remains
associated with water
• Sodium-containing fluids are distributed throughout the ECF and add to the
volume of both the intravascular and interstitial spaces (3 times as much as
the plasma)
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Cont.

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 Osmotic Pressure
• The physiologic activity of electrolytes in solution
depends on:
– The number of particles per unit volume (millimoles
per liter, or mmol/L)
– The number of electric charges per unit volume
(milliequivalents per liter, or mEq/L)
– The number of osmotically active ions per unit volume
(milliosmoles per liter, or mOsm/L)
• For example, 1 mmol of sodium chloride contributes to 2
mOsm (one from sodium and one from chloride)

7
 Cont.
• The concentration of electrolytes usually is
expressed in terms of the chemical combining
activity, or equivalents
– An equivalent of an ion is its atomic weight
expressed in grams divided by the valence
• Equivalent = atomic weight (g)/valence
– For univalent ions such as sodium, 1 mEq is the
same as 1 mmol
• For divalent ions such as magnesium, 1 mmol equals 2
mEq
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 Cont.
• The principal determinants of osmolality are the
concentrations of sodium, glucose, and urea
(BUN)
– Calculated serum osmolality = 2 sodium +
(glucose/18) + (BUN/2.8)

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 Cont.
• The osmolality of the intracellular and extracellular fluids is
maintained between 290 and 310 mOsm in each compartment

• Because cell membranes are permeable to water, any change

in osmotic pressure in one compartment is accompanied by a
redistribution of water until the effective osmotic pressure
between compartments is equal

• Most significant gains and losses of body fluid are directly from
the extracellular compartment

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 Body fluid changes
• The healthy person consumes an average of 2000 mL of water
per day, approximately 75% from oral intake and the rest
extracted from solid foods

• Daily water losses include 800 to 1200 mL in urine, 250 mL in

stool, and 600 mL in insensible losses
– Insensible losses of water occur through both the skin (75%) and lungs
(25%)

• To clear the products of metabolism, the kidneys must excrete

a minimum of 500 to 800 mL of urine per day, regardless of the
amount of oral intake
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 Cont.
• Composition of GI secretions

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 Disturbances in Fluid Balance
• 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 CVS and CNS
signs
– Chronic deficits display tissue signs, such as a
decrease in skin turgor and sunken eyes, in addition
to CVS and CNS signs

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 Cont.
• The most common cause of volume deficit in
surgical patients is a loss of GI fluids from NG
suction, vomiting, diarrhea, or enterocutaneous
fistula
– Other
• Sequestration secondary to soft tissue injuries, burns
• Intra-abdominal processes such as peritonitis,
obstruction, or prolonged surgery

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 Cont.
• Serum sodium concentration does not
necessarily reflect volume status and therefore
may be high, normal, or low when a volume
deficit is present

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 Volume Control
• Volume changes are sensed by both osmoreceptors and
baroreceptors
– Osmoreceptors are specialized sensors that detect small
changes in fluid osmolality
• Drive changes in thirst and diuresis through the kidneys
• Vasopressin is secreted and results in water reabsorption in the
kidneys
– Baroreceptors
• Responses are both neural, through sympathetic and
parasympathetic pathways, and hormonal, through substances
including renin-angiotensin, aldosterone, ANP, and renal
prostaglandins

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Fluid therapy

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 Parenteral Solutions
• Both lactated Ringer’s solution and normal saline are
considered isotonic
– Lactated Ringer’s is slightly hypotonic
• Lactate is used rather than bicarbonate because it is more stable
in IV fluids during storage
– It is converted into bicarbonate by the liver after infusion, even in the face
of hemorrhagic shock
– Sodium chloride is mildly hypertonic
• It is an ideal solution for correcting volume deficits associated with
hyponatremia, hypochloremia, and metabolic alkalosis
• The high chloride concentration imposes a significant chloride
load on the kidneys and may lead to a hyperchloremic metabolic
acidosis
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 Cont.

Colloids: albumin, dextrans, hetastarch, and gelatins

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 Preoperative Fluid Therapy
• The administration of maintenance fluids should
be all that is required in an otherwise healthy
individual who may be under orders to receive
nothing by mouth for some period before the
time of surgery

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 Cont.
• Although there should be no “routine”
maintenance fluid orders, an appropriate choice
of 5% dextrose in 0.45% sodium chloride at 100
mL/h should be used as initial therapy, with
potassium added for patients with normal renal
function
– However, many surgical patients have volume
and/or electrolyte abnormalities associated with
their surgical disease

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 Intraoperative 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
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 Cont.
• 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
– These represent distributional shifts, in that the
functional volume of ECF is reduced but fluid is not
externally lost from the body

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 Cont.
• Preoperative FD + MF + 3rd space loss + EBL

– Fluid (NPO) deficit = Number of hours NPO x MF

– In the first hour of surgery 50 % of the Preoperative FD
should be replaced, and 25 % during each of the second
and third hours
– Fluids used intra-op should be isotonic (NS/RL)
• Replace 3cc of crystalloid solution per cc of blood loss
• When using blood products or colloids replace blood loss volume
per volume
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Intra-operative fluid therapy

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 Cont.
• Example
– 62 years old male, 80 kg, for hemicolectomy
– NPO after 22:00, surgery at 08:00, received bowel prep
– 3 hr. procedure, 500 cc blood loss
– What are his estimated intraoperative fluid requirements?

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 Example (cont.)
• Cont.
– Fluid deficit (NPO): 102ml/hr x 10 hrs = 1020 ml + 1000 ml
for bowel prep = 2020 ml total deficit
• To be replaced 1/2 first hr, 1/4 2nd hr, 1/4 3rd hour
– Maintenance: 102ml/hr x 3hrs = 306ml
– Third Space Losses: 6ml/kg/hr x 3 hrs =1440 ml
– Blood Loss: 500ml x 3 = 1500ml
– Total = 2020+306+1440+1500=5266ml

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 Postoperative fluid therapy
• It 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
– Preoperative or intraoperative FD + MF + OL
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 Cont.
• In the initial postoperative period, an isotonic
solution should be administered

• After the initial 24 to 48 hours, fluids can be

changed to 5% dextrose in 0.45% saline in patients
unable to tolerate enteral nutrition
– If normal renal function and adequate urine output are
present, potassium may be added to the IV fluids
– All losses, including losses through vomiting, NG
suctioning, drains, and urine output should be replaced
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 Cont.
• The administration of isotonic fluids in excess of
actual needs may result in excess volume
expansion
– The earliest sign of volume overload is weight gain
• The average postoperative patient who is not receiving
nutritional support should lose approximately 0.25 to 0.5
lb/d (0.11 to 0.23 kg/d) from catabolism

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Electrolyte changes

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 Hyponatremia
• Extracellular volume can be high, normal, or low

• In most cases of hyponatremia, sodium concentration is decreased

as a consequence of either sodium depletion or dilution

• Dilutional hyponatremia
– Excessive oral water intake or iatrogenic intravenous IV excess free
water administration
– Post-op patients are particularly prone to increased secretion of ADH,
which increases reabsorption of free water from the kidneys with
subsequent volume expansion and hyponatremia
• This is usually self-limiting in that both hyponatremia and volume expansion
decrease ADH secretion
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 Cont.
• Depletional causes of hyponatremia are associated
with either a decreased intake or increased loss of
sodium-containing fluids (concomitant ECF volume
deficit is common)
– Decreased sodium intake
• Consumption of a low-sodium diet or use of enteral feeds,
which are typically low in sodium
– GI losses
• Vomiting, prolonged NG suctioning, or diarrhea
– Renal losses
• Diuretic use or primary renal disease
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 Cont.
• Hyponatremia also can be seen with an excess
of solute relative to free water, such as with
untreated hyperglycemia or mannitol
administration
– Glucose exerts an osmotic force in the extracellular
compartment, causing a shift of water from the
intracellular to the extracellular space
• For every 100-mg/dL increment in plasma glucose above
normal, the plasma sodium should decrease by 1.6 mEq/L

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Cont.

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 Cont.
• Clinical features
– In patients with normal renal function, symptomatic
hyponatremia usually does not occur until the serum
sodium level is ≤120 mEq/L
– Signs and symptoms of hyponatremia are dependent on the
degree of hyponatremia and the rapidity with which it
occurred
– Clinical manifestations primarily have a CNS origin and are
related to cellular water intoxication and associated
increases in intracranial pressure
– N/V and headache are the earliest symptoms
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Cont.

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 Cont.
• Treatment
– Most cases can be treated by free water restriction and, if severe,
the administration of sodium
– If neurologic symptoms are present, 3% normal saline should be
used to increase the sodium by no more than 1 mEq/L/hr until the
serum sodium level reaches 130 mEq/L or neurologic symptoms
are improved
– Correction of asymptomatic and/or chronic hyponatremia should
increase the sodium level by no more than 0.5 mEq/L/hr to a
maximum increase of 12 mEq/L/day
• Rapid correction can lead to pontine myelinolysis
– Seizures, weakness, paresis, akinetic movements, unresponsiveness, permanent brain
damage, and finally death
– Sodium deficit = (Nameasured – Natarget) × TBW
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 Hypernatremia
• It results from either a loss of free water or a
gain of sodium in excess of water

• Like hyponatremia, it can be associated with an

increased, normal, or decreased extracellular
volume

• It is less common than hyponatremia, but has a

worse prognosis
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 Cont.
• Hypervolemic hypernatremia
– Iatrogenic administration of sodium-containing fluids
– Mineralocorticoid excess
• Hyperaldosteronism, Cushing’s syndrome, and congenital adrenal hyperplasia
• Normovolemic hypernatremia
– Renal causes, including diabetes insipidus, diuretic use, and renal
disease
– Non-renal water loss from the GI tract or skin
• Hypovolemic
– Non-renal water loss
• Relatively isotonic GI fluid losses such as that caused by diarrhea
– Hypotonic skin fluid losses such as loss due to fever
– Losses via tracheotomies during hyperventilation 40
Cont.

41
 Cont.
• Clinical features
– Symptomatic hypernatremia usually occurs only in
patients with impaired thirst or restricted access to
fluid, because thirst will result in increased water intake
– Symptoms are rare until the serum sodium
concentration exceeds 160 mEq/L but, once present,
are associated with significant morbidity and mortality
– CNS effects predominate (restlessness, irritability,
seizures, coma, and death)
• As a result of cellular dehydration
– This can put traction on the cerebral vessels and lead to SAH
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Cont.

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 Cont.
• Treatment
– Usually consists of treatment of the associated
water deficit
– Water deficit (L) = Serum sodium - 140 × TBW
140
• Estimate TBW as 50% of lean body mass in men and
40% in women

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 Cont.
• Cont.
– In hypovolemic patients, volume should be restored with normal
saline before the concentration abnormality is addressed
• Once adequate volume has been achieved, the water deficit is replaced
using a hypotonic fluid such as 5% dextrose
– Rate of fluid administration should be titrated to achieve a decrease
in serum sodium concentration of no more than 1 mEq/h and 12
mEq/d for the treatment of acute symptomatic hypernatremia
• Even slower correction should be undertaken for chronic hypernatremia (0.7
mEq/h), because overly rapid correction can lead to cerebral edema and
herniation
– Frequent neurologic evaluation as well as frequent evaluation of
serum sodium levels should be performed
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 Hyperkalemia
• It is caused by:
– Excessive potassium intake
• Oral or IV supplementation
– Increased release of potassium from cells (98% of
total body potassium is intracellular)
• Hemolysis, rhabdomyolysis, and crush injuries
• Acidosis and a rapid rise in extracellular osmolality from
hyperglycemia or IV mannitol
– Shift of potassium ions to the extracellular compartment
– Impaired potassium excretion by the kidneys
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 Cont.
• Clinical features
– GI
• Nausea, vomiting, intestinal colic, and diarrhea
– Neuromuscular
• Range from weakness to ascending paralysis to respiratory
failure
– Cardiovascular
• Early: ECG changes
– High peaked T waves (early), widened QRS complex, flattened P wave,
prolonged PR interval (first-degree block), sine wave formation, and
ventricular fibrillation
• Late: hemodynamic symptoms of arrhythmia and cardiac arrest
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 Cont.
• Treatment
– Shift potassium
• Glucose 1 ampule of D-50 and regular insulin 5–10 units IV
• Bicarbonate 1 ampule IV
• Nebulized albuterol 10 to 20 mg
– Potassium removal
• Kayexalate
– Oral administration: 15–30 g in 50–100 mL of 20% sorbitol
– Rectal administration: 50 g in 200 mL of 20% sorbitol
• Loop diuretics (kaliuresis)
• Dialysis
– Should be considered when conservative measures fail
– Counteract cardiac effects
• Calcium gluconate 5–10 mL of 10% solution
– When ECG changes are present 48
 Hypokalemia
• It is much more common than hyperkalemia in the
surgical patient
• Causes
– Inadequate potassium intake
– Loss
• Potassium loss in pathologic GI secretions, such as with
diarrhea, fistulas, vomiting, or high NG output
• Excessive renal potassium excretion
– Intracellular shifts
• From metabolic alkalosis or insulin therapy
– Potassium decreases by 0.3 mEq/L for every 0.1 increase in pH above
normal
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 Cont.
• Clinical features
– GI
• Ileus, constipation
– NM
• Weakness, fatigue, diminished tendon reflexes, paralysis
– CVS
• ECG changes: U waves, T-wave flattening, ST-segment
changes (depression), and arrhythmias
• Cardiac arrest

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 Cont.
• Treatment
– Repletion of potassium, the rate of which is
determined by the symptoms
• Oral repletion is adequate for mild, asymptomatic
hypokalemia
• If IV repletion is required, usually no more than 10 mEq/h
is advisable in an unmonitored setting
– This amount can be increased to 40 mEq/h when accompanied
by continuous ECG monitoring

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 Hypocalcemia
• The vast majority of the body’s calcium is
contained within the bone matrix, with <1%
found in the ECF

• Serum calcium is distributed among three forms:

– Ionized (50%)
• It is this fractions which is responsible for neuromuscular
stability and can be measured directly
– Protein found (40%)
– Complexed to phosphate and other anions (10%)
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 Cont.
• Total serum calcium levels are affected by albumin
concentration
– Adjust total serum calcium down by 0.8 mg/dL for every 1
g/dL decrease in albumin

• Unlike changes in albumin, changes in pH will affect

the ionized calcium concentration
– Acidosis decreases protein binding, thereby increasing the
ionized fraction of calcium
– The reverse is true during alkalosis

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 Cont.
• Causes of hypocalcemia
– Massive soft tissue infections such as necrotizing fasciitis
– Pancreatitis
• Sequesteration of calcium via chelation with free fatty acids
– Pancreatic and small bowel fistulas
– Renal failure
– Hypoparathyroidism
– Toxic shock syndrome
– Tumor lysis syndrome
– Abnormalities in magnesium levels
Hypocalcemia rarely results solely from decrease intake, because bone
reabsorption can maintain normal level for prolonged periods 54
 Cont.
• Clinical features
– Symptoms do not occur until the ionized fraction
falls below 2.5 mg/dL
• Neurologic: Paresthesias of the face and extremities,
muscle cramps, carpopedal spasm, stridor, tetany, and
seizures
– Chvostek’s sign
– Trousseau’s sign
• CVS
– Decreased cardiac contractility and heart failure
– ECG changes: prolonged QT interval, T-wave inversion, heart
block, and ventricular fibrillation
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 Cont.
• Treatment
– Acute symptomatic hypocalcemia should be treated
with IV 10% calcium gluconate
– Asymptomatic hypocalcemia can be treated with
oral or IV calcium
– Associated deficits in magnesium, potassium, and
pH must also be corrected

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 Hypercalcemia
• Causes
– Outpatient
• Primary hyperparathyroidism
– Hospitalized
• Malignancy
– Bony metastasis

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 Cont.
• Clinical features
– GI
• Nausea, vomiting, and abdominal pain
– Neurologic
• Neurologic impairment, musculoskeletal weakness and
pain, renal dysfunction
– CVS
• Hypertension
• ECG changes
– Shortened QT interval, prolonged PR and QRS intervals, increased
QRS voltage, T-wave flattening and widening, and AV block (which
can progress to complete heart block and cardiac arrest)
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 Cont.
• Treatment
– Treatment is required when it is symptomatic
– The initial treatment is aimed at repleting the
associated volume deficit and then inducing a brisk
diuresis with normal saline

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 Hypomagnesemia
• Approximately one half of the total body content is
incorporated in bone and is slowly exchangeable
• Of the fraction found in the extracellular space, one third is
bound to serum albumin
– Therefore, the plasma level of magnesium may be a poor
indicator of total body stores in the presence of hypoalbuminemia
• The kidney is primarily responsible for magnesium
homeostasis through regulation by calcium/magnesium
receptors on the renal tubular cells that respond to serum
magnesium concentrations

60
 Cont.
• Causes
– Poor intake
– Excess renal excretion
– Pathologic losses
• Diarrhea, malabsorption, and acute pancreatitis

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 Cont.
• Clinical features
– Symptoms are similar to those of calcium deficiency
• Hyperactive reflexes, muscle tremors, tetany, and positive
Chvostek’s and Trousseau’s signs
– Severe deficiencies can lead to delirium and seizures
• ECG changes: prolonged QT and PR intervals, ST-segment
depression, flattening or inversion of P waves, torsades
de pointes, and arrhythmias
– Hypomagnesemia can produce hypocalcemia and
lead to persistent hypokalemia

62
 Cont.
• Treatment
– Severe deficits (<1.0 mEq/L) or Symptomatic
• 1 to 2 g of magnesium sulfate may be administered IV
over 15 minute
• Simultaneous administration of calcium gluconate
– It will counteract the adverse side effects of a rapidly rising
magnesium level and correct hypocalcemia, which is frequently
associated with hypomagnesemia
– Correction can be oral if asymptomatic and mild

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Electrolyte disturbances in
specific surgical patients

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 Neurologic Patients
• SIADH
– It can occur after head injury or surgery to the CNS
• Also seen in small cell cancer of the lung, pancreatic
carcinoma, and thymoma
– It should be considered in patients who are
euvolemic and hyponatremic with elevated urine
sodium levels and urine osmolality
– In most cases, restriction of free water will improve
the hyponatremia
• Furosemide also can be used to induce free water loss
65
 Cont.
• Diabetes Insipidus
– It is a disorder of ADH stimulation and is manifested
by dilute urine in the case of hypernatremia
– Types
• Central DI results from a defect in ADH secretion
– Pituitary surgery, closed head injury, and anoxic encephalopathy
• Nephrogenic DI results from a defect in end-organ
responsiveness to ADH
– Hypokalemia, radiocontrast dye, Certain drugs (aminoglycosides
and amphotericin)

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 Cont.
• Cont.
– Volume depletion can occur rapidly in patients
incapable of oral intake
– Diagnosis can be confirmed by documenting a
paradoxical increase in urine osmolality in response
to a period of water deprivation
– In mild cases, free water replacement may be
adequate therapy
• In more severe cases, vasopressin can be added

67
 Malnourished Patients
• Refeeding Syndrome
– It is a potentially lethal condition that can occur with rapid and
excessive feeding of patients with severe underlying malnutrition
– With refeeding, a shift in metabolism from fat to carbohydrate
substrate stimulates insulin release, which results in the cellular
uptake of electrolytes
• Paradoxically, severe hyperglycemia may result from blunted basal insulin
secretion
– Symptoms from electrolyte abnormalities may ensue
– Prevention and treatment
• Caloric repletion should be instituted slowly and should gradually increase
over the first week
• Thiamine should be administered before the initiation of feeding
• Any electrolyte abnormalities should be corrected
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 Acute renal failure
• Hyperkalemia
• Hyponatremia
• Hypocalcemia
• Hypermagnesemia
• Hyperphosphatemia
• Metabolic acidosis

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Acid-Base Balance

70
 Acid-Base Homeostasis
• The pH of body fluids is maintained within a
narrow range (7.35 – 7.45) despite the ability of
the kidneys to generate large amounts of HCO3−
and the normal large acid load produced as a
byproduct of metabolism

• Important buffers include intracellular proteins

and phosphates and the extracellular
bicarbonate–carbonic acid system
71
 Cont.
• Compensation for acid-base derangements can be by
respiratory mechanisms (for metabolic derangements) or
metabolic mechanisms (for respiratory derangements)
– Changes in ventilation in response to metabolic abnormalities are
mediated by hydrogensensitive chemoreceptors found in the
carotid body and brain stem
– The kidneys provide compensation for respiratory abnormalities
by either increasing or decreasing bicarbonate reabsorption in
response to respiratory acidosis or alkalosis, respectively
• The compensatory response in the kidneys to respiratory abnormalities is
delayed, unlike the respiratory compensation to metabolic abnormalities
– Significant compensation may not begin for 6 hours and then may continue for
several days

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 Metabolic Acidosis
• It results from
– Increased intake of acids
– Increased generation of acids
– Increased loss of bicarbonate
• The body responds by several mechanisms
– Producing buffers
– Increasing ventilation (Kussmaul’s respirations)
– Increasing renal reabsorption and generation of
bicarbonate
• The kidneys also will increase secretion of hydrogen
73
 Cont.
• Evaluation includes determination of the anion
gap (AG), an index of unmeasured anions
– AG = (Na) – (Cl + HCO3)

– The normal AG is <12 mmol/L

74
 Cont.
• Increased AG occurs
– Ingestion of exogenous acid
• Ethylene glycol, salicylates, or methanol
– Increased endogenous acid production
• β-Hydroxybutyrate and acetoacetate in ketoacidosis
• Lactate in lactic acidosis
• Organic acids in renal insufficiency

75
 Cont.
• Normal AG (bicarbonate loss is accompanied by
a gain of chloride)
– Exogenous acid administration
• HCl
• NH4+
– Loss of bicarbonate
• GI disorders
– Diarrhea, fistulas, ureterosigmoidostomy
• Renal losses
– Renal tubular acidosis

76
 Cont.
• A common cause of severe metabolic acidosis
in surgical patients is lactic acidosis
– Lactate is produced in the presence of hypoxia from
inadequate tissue perfusion
– The treatment is to restore perfusion with volume
resuscitation rather than to attempt to correct the
abnormality with exogenous bicarbonate

77
 Metabolic alkalosis
• It 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–

• Hypochloremic and hypokalemic metabolic alkalosis can

occur from isolated loss of gastric contents
78
 Respiratory Acidosis
• It is associated with the retention of CO2
secondary to decreased alveolar ventilation
– Pulmonary pathologies, thoracic and upper
abdominal incisions, intra-abdominal pathologies,
narcotics, CNS injury

• Treatment of acute respiratory acidosis is

directed at the underlying cause with measures
to ensure adequate ventilation
79
 Respiratory Alkalosis
• In the surgical patient, most cases of
respiratory alkalosis are acute and secondary
to alveolar hyperventilation
– Pain, anxiety, assisted ventilation, and neurologic
disorders (CNS injury)

• Treatment should be directed at the

underlying cause

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End!

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