22.07.

2010

Fluid and electrolyte disturbances

at surgical patients

Many pathological surgical conditions such as bowel

obstruction, hemorrhage,
obstruction hemorrhage burns,
burns pancreatitis,
pancreatitis peritonitis,
peritonitis pyloric
stenosis, etc. or a surgical intervention may lead to acute
alteration in the volume and composition (concentration of
important electrolytes) of fluid. Precise perioperative
management of fluids and electrolytes is thus required to
minimize pperioperative
p morbidityy and mortality.
y

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 22.07.2010

Total Body Water (TBW) 60%

or 42L in 70 kg person.

Extracellular (ECV) 20 %
ntracellular ((ICV)) 40%
or 14L off TBW
or 28L of TBW

travascular ((PV)) 25% or 3,5L

, Interstitial (IF) 75 %
(5% of TBW) 10,5L (15% of TBW)

Red cell volume 2-3%

or 1,5L of TBW

Total Body Water

body wt% Total body
water%
total 60 100
intracellular 40 67
extracellular 20 33
intravas 5 8
interstitial 15 25

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 22.07.2010

The solute and colloid compositions of the

EC and IC fluid compartments differ markedly.

Composition of Fluids
plasma interstitial intracellular
Cations
Na 140 146 12
K 4 4 150
Ca 5 3 10
Mg 2 1 7
Anions
Cl 103 104 3
HCO 24 27 10
SO4 1 1 -
HPO4 2 2 116
Protein 16 5 40

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 22.07.2010

The solute and colloid compositions of the EC and IC fluid compartments

 Sodium concentration in the PV is higher (135-145 ) versus ICF.

 The predominant intracellular cation is potassium (serum
concentration is app. 3,5-5,3)
 Albumin represents the most important osmoticaly active
constituent of the ECV; serum concentration is 4,0 g/dL .
 TBW is the distribution volume for sodium-free water;
 ECV is the distribution for crystalloid solution
 Whereas PV represents the distribution volume for most colloid
solutions.

Intracellular volume 40%

or 28L of TBW
distribution volume for sodium-free water (D5W)

Interstitial volume 10,5L (5% of TBW)

distribution for crystalloid solutions

Intravascular volume (plasma – 3,5L with RBC – 1,5L) 5L (7-8% of TBW)

distribution volume for most colloid solutions (albumin)

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 22.07.2010

 Assume a 70kg patient has suffered an acute blood loss of 1000ml,

approximately
pp y 20% of p
predicted 5L blood volume.
An one of 5% dextrose in water (D5W), lactated Ringer's solution, or 5%
albumin may by chosen to replace the lost blood volume.
To restore blood volume using D5W which distributes throughout TBW
(42L) it would be necessary to administer 12L.
Lactated Ringer's solution would require approximately 4L of crystalloid
solution.
Colloide solutions with similar oncotic pressures to plasma (5% albumin)
distribute within the intravascular space and thus have the distribution
volume equal to the plasma volume. In this example, 1L of albumin
solution would be required to replace the shed blood.

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 22.07.2010

Normal Water Exchange (water intake and loses)

Represent normal basic requirements of fluid to any person
Normal fluid loses Avg daily ml
Sensible
Urine 800-1500;
I
Intestinal
i l 00-250;
250
Insensible
lungs/skin 600-900; app. 8-12ml/kg/day equally divided into respiratory
and cutaneus water loses;
Note.  10%/ o rise in Temp;
Approximately
pp y 2,5L p per day,
y or 35-40 ml/kg/day)
g y)
Normal fluid Intake of Water
2000mls: - 1300 free water; 700 bound to food

additional water comes from catabolism

Volume control and response of the neuroendocrine system to dehydration.

1) Osmoreceptor cells in paraventricular/supraoptic nuclei control thirst
and ADH secretion.
2) Baroreceptors in carotic sinus and arch of the aorta are sensitive to
decreased circulating volume (tachycardia)

- Synthesis of the renin by the juxtaglomerular apparatus is a response to

decreased circulating volume. Renin activates angiotensin I, which is
converted to angiotensin II, a potent vasoconstrictor. It also stimulates
aldosteron and ADH secretion.
- Aldosteron acts on the renal tubules to conserve Na+.
- ADH - fluid retention.
- Final result is an increase in sympathetic activity, release of stress
hormones, reabsorption of interstitial fluid, conservation of fluids and
electrolytes by kidneys.

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 22.07.2010

Dehydration - etiology

 1) Hemorrhage: intravascular volume depletion

 2) Surgical patients: nil orally, anesthesia, trauma, sepsis
 3) Loss of plasma volume through a) GIT, b) insensible losses, c) urinary,
or d) extravascular volume sequestration:
a) Gastrointestinal loses: prolonged vomiting, severe diarrhea,
b) Excessive insensible loses: caused by fever (perspiration),
hyperventilation, and burns.
c) Urinary loses: diabetes insipidus, loop diuretics.
d) Extravascular volume sequestration or "third space" fluid losses
- as a result
l off llocall iinflammation
fl i process ((pancreatitis)
i i ) lleading
di to change
h
in permeability resulting in fluid extravasation from the intravascular
space to the interstitium.
- small bowel obstruction. In this case hypovolemia results from fluid loss
into the interstitium, bowel lumen and exudation of the fluid into the
peritoneal cavity.

Diagnosis of fluid-electrolyte disturbances.

1. History of fluid losses:
external losses such as bleeding, melena, vomiting, diarrhea are obvious;
internal losses such as lost into obstructed bowel, pancreatitis, or internal
bleeding may be subtle;

2. Physical examination:
Vital signs (heart rate, blood pressure), weight change, skin turgor, moistness
of mucous membranes, venous filling, urine output (UO);

3. Laboratory tests: hematocrit (Ht), serum Na, K, HCO3, Cl, and glucose;
blood urea nitrogen (BUN) and creatinine.
Other tests if needed – serum osmolality 285
285-295
295 mOsm/L
Posm = 2x serum [Na] + glocose/18 + BUN/2.8;
Urine osmolality;

4. Indirect measurement of circulating volume: CVP, PAWP may be useful for

diagnosis or to guide rehydration.

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 22.07.2010

skin turgor examination

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 22.07.2010

Clinical calculation and correction of the I. existing deficit

 Mild dehydration (1st degree 3% of TBWeight): thirst
 Moderate dehydration (2nd degree 6% of TBW): marked thirst and dry
mucous membranes (groin, armpit), loss of skin turgor;
 Severe dehydration (3rd degree 10% of TBW): plus orthostatic hypotension,
confusion, or delirious. Sunken eyes.
 Progressive changes of the following values: heart rate increases, CVP
decreases, urine output low (oliguria)

Estimation of existing deficit and its correction has top priority. It is

evaluated using clinical picture and vital signs.

Management
Replace half of the calculated deficit quickly (over 12-24 hours),
then re-examine the patient and reassess the need for further
deficit correction. Composition of used for therapy solutions
has to take into account an etiology of deficit.

A 70 kg women has been suffering by prolonged

vomiting for two days. She complaints of marked
thirst. Examining the patient the following signs are
found: dry tongue, loss of skin turgor, increased heart
rate, 90 mmHg blood pressure at upright position,
urine output is 300 ml/daily.

Q
Questions:
 How much fluid (water) and what i.v. solution does
she need to cover existing deficit?

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 22.07.2010

II. Ongoing Losses

represent continuing losses from or within the body.
Etiology NG, drains, fistulae, stomas, third space losses

Management
Replacement of ongoing loses (so-called replacement therapy) has second
priority in F/E treatment. It is done with fluids possessing approximately
similar composition to lost one.

Gastric losses are replaced

p using
g 0,45%
, NaCl p
plus 20-30 mEq
q KCl/L
/

Intestinal juice is replaced with lactated Ringer’s solution plus 10 mEq KCl/L;

Third space losses are most difficult to evaluate, they vary with magnitude of
the injury. Lactated Ringer’s solution or normal saline plus albumin is used
for replacement.

 a 100 kg men has had an elective resection of a part of

the
h bbowel.l Th
The patient
i h has ddeveloped
l d paralytic
l i ilileus.
To decompress the GIT a nasogastric tube is inserted.
Over the next 24 hours, there is a 1000ml of
nasogastric drainage. Serum electrolytes are normal.
Q
Questions:
 How much fluid (water) does he need to cover
ongoing loses?

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III. Maintenance (basic) requirements of fluid

Maintenance requirements are defined as the fluid and electrolytes

necessary to maintain daily fluid and electrolyte balance in an individual.
This includes usual daily fluid losses: insensible, urinary, and stool.
Common average daily requirements for fluid are 35-40 ml/kg.

Maintenance solution D5W + 1/2 NS or 2/3 D5W +1/2 NS. Potassium is

often added to this solutions at concentration approximating 20 mEq/L.

Maintenance electrolyte requirements

Na 1-2mEq/Kg/d
q/ g/
K 0.5 - 1 mEq/Kg/d
 Usually no K given until after urine output is adequate
 Always give K with care, in an infusion slowly - never bolus
 Ca, PO4, Mg not required for short term

a 70 kg women has had an elective cholecystectomy.

Q
Questions:
i
 How much fluid (water) does she need at first postoperative
day?
 What i.v. solution (s) is (are) to be ordered during first
postoperative day?
 What i.v. solution (s) is (are) to be ordered during second
postoperative day if circumstances are the same?

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 22.07.2010

Fluid and electrolyte therapy

Surgical patients have
 Volume deficits (existing deficit): estimate using vital signs
 On going losses: measure all losses in I/O chart, estimate third space
losses
 Maintenance requirements: use BW formula
 Maintenance electrolyte requirements: use lab values
 Electrolyte excess/deficits: use lab values

Thee best estimate

est ate of
o the
t e volume
vo u e required
equ ed iss the
t e patients
pat e ts response
espo se

a 100 kg men has had an emergency surgery - resection of 2/3 of the

stomach (Billirot II type of resection) due to peptic ulcer complicated
by internal bleeding (1000ml of blood has been lost). The patient has
developed paralytic ileus. To decompress the GIT a nasogastric tube
is inserted. Over the next 24 hours, there is a 500ml of nonstained
nasogastric drainage. Serum electrolytes are normal.
 Q ti n :
Questions:
 What is a total volume of fluid needed at first postoperative day?
 How much fluid (water) does he need to cover maintenance daily
requirements?
 How much fluid (water) does he need to cover ongoing loses?
 What i.v. solution (s) and how much is administered to cover existingg
deficit
 What i.v. solution (s) and how much is (are) to be ordered during first
postoperative day?

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Perioperative fluid requirements (esp. for NPO patients)

 The amount of fluids administered in the postoperative period (within the

first 12-24h) must take into account the existing deficit, maintenance
requirements and any ongoing loses. The preferred approach of
postoperative fluid orders is to reassess the patient frequently to determine
intravascular volume status.
status
 Evaluation of vital signs (heart rate, BP) and most importantly hourly
urine output(0.5 - 1ml/Kg/hr) provide an excellent measure of
intravascular volume status. Urine specific gravity may be used (1.010 -
1.012), CVP is useful in difficult situations (5-15 cm H2O). Sometime
PAWP may be useful to guide rehydration. Body weight measured in
special situation e.g. burns

 It has become common practice to avoid potassium supplementation

within the first 24h. The preferred practice is to administer normal saline or
lactated Ringer's solution in the first 24h. At the first postoperative
morning, these solutions are switched to dextrose containing solutions
(D5W + 1/2 NS or 2/3 D5W +1/2 NS) supplemented with KCL providing
that urine output has become adequate.

Commonly used parenteral solutions

Electrolyte content, mEq/L

 0,9% NaCl (NS): 154 of Na + and 154 of Cl -
 0,45% NaCl (1/2 NS): 77 of Na + and 77 of Cl -
 0 27% NaCl (1/4 NS): 38 of Na + and 38 of Cl -
0,27%
 LR: 130 of Na +, 109 of Cl, 4 of K +, 28 of HCO3 -, 3 of Ca 2+.
 D5W: does not contain any electrolytes (it’s almost a free water);

Electrolyte content, mEq/dL

 3% NaCl: 51 of Na + and 51 of Cl –
 5% NaCl: 85 of Na + and 85 of Cl -
Electrolyte content, mEq/ampul
 14,9% KCl (ampule): contains 40 mEq of K +, and 40 mEq of Cl - ;
 7,5 % NaHCO3- : contains 44,6 mEq of Na +, and 44,6 mEq of HCO3- ;

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Commonly used parenteral solutions

 0,9% NaCl (NS): ECF replacement, correction of hyponatremia.
 0,45% NaCl (1/2 NS): Na maintenance, gastric fluid replacement.
 0,27% NaCl (1/4 NS): as for D5W.
 LR: best ECF replacement,
p , correction of isotonic deficit.
 D5W: correction of insensible water loss, correction of hyperosmolar
dehydration. Overuse will cause dilutional hyponatremia.

 3% NaCl: correction of symptomatic Na deficit, 510 mEq/L;

 5% NaCl: correction of symptomatic Na deficit, 850 mEq/L;

 14,9% KCl (ampule): additive for K maintenance and imbalance. Never add
more than 40 mEq to each liter of fluid.

 7,5 % NaHCO3- : additive for GI losses, correction of metabolic acidosis.

Disorders of sodium homeostasis

Physiology
 The p
plasma [[Na+] is the major
j determinant of Posm (as
( a glucose).
g )
Maintenance of plasma osmolality: ability of the kidneys to excrete water
and on a normal thirst mechanism. Antidiuretic hormone (ADH) is a
principal regulator of serum osmolality.

Hyponatremia
 The approach to the hyponatremia begins with the assessment of serum
osmolality. If serum osmolality is high
g it is important
p to consider the
possibility of other effective plasma osmoles, the most common of which
is glucose. Hyperglycemia shifts water from the cells leading to dilutional
hyponatremia (treatment include administration of insulin and fluid
replenishment).

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 22.07.2010

Hyponatremia
More frequently a low [Na+] will be associated with reduced plasma osmolality

 A reduction in extracellular volume (plasma, gastric loses, administration

of Na-free solutions). It is due to Na+ loss. The treatment involves
replenishment the extravascular volume with isotonic solutions in
concert with restriction of free water.
water

 Hyponatremia in the presence of increased EVV (dilutional

hyponatremia). This represents edematous states (such as low cardiac
output states, cirrhosis, hypoalbuminemic states). Both water restriction
and sodium restriction are necessary. Loop diuretic may be required to
increase both water and sodium loss. This induce of excess of urinary
water loss over Na+ loss and should correct hyponatremia.
yp

 Patients with a normal ECV may have the syndrome of inappropriate

ADH secretion. It causes overconservation of free water. The treatment is
water restriction.

 Symptoms of increased intracranial pressure from cerebral edema are the

most prominent feature. Too rapid correction of plasma Na may result in
central pontine myelinosis caused by cell shrinkage that may result in
irreversible brain stem injury. Correction with 3% NaCl 0,5mEq/L per
hour.
 F
Features depend
d d on rapidity
idi
acute drop below 120
weakness
fatigue
confusion
cramps
nausea/vomiting
headache/delirium/seizures/coma
permanent CNS damage

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Hypernatremia (more than 150mEq/L)

Etiology
 Elevated plasma [Na+] occurs as a result of excessive free water loss, and
is thus frequently associated with hypovolemia and oliguria. Excessive
insensible loses caused by fever, hyperventilation, and burns, or hypotonic
fluid loses due to p
perspiration,
p , or severe diarrhea are the p
principal
p causes.
 Osmotic diuresis induced by hyperglycemia or mannitol may cause
profound hypernatremia. Central diabetes insipidus following
neurosurgical operations or head injury.

Clinical picture and pathophysiology

Cellular shrinkage caused by fluid shift from the IC space to the EC
compartment may cause confusion
confusion, coma,
coma and intracranial hemorrhage.
hemorrhage

Treatment
 Rapid correction may cause irreversible neurological deficit. Sufficient free
water should by administered to reduce plasma Na.

Disorders of potassium homeostasis

Physiology
 Potassium is a major intracellular cation. Only 2% of total body potassium
is located in the EC fluid. Slight alterations in plasma [K] may have
dramatic effects on muscle contraction and nerve conduction as the
concentration
n ntr ti n gradient
r di nt across
r the
th plasma
pl m membrane
m mbr n is i the
th main
m in
determinant of the membrane excitability.

Hypokalemia
 Hypokalemia in surgical patients is mainly due to losses from GIT,
kidneys, or skin. Diarrhea, vomiting and massive burns may also cause
hypokalemia because of combination of tissue breakdown and fluid loss.
The major danger associated with hypokalemia is cardiac arrhythmia.
arrhythmia
 Too rapid correction may result in hyperkalemia because it takes time for
the administered K to be transferred into cells. When possible, K
supplementation should by administered orally. Potassium can be
administered i.v. with administration rate no grate than 20-40 mEq/L per
hour, with continuous ECG monitoring.

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 22.07.2010

Hyperkalemia

 Sudden increase in [K+] are almost always caused by rapid administration

of K+. By contrast, sustained hyperkalemia implies that there is
impairment of renal K+ excretion. Transcellular flux of K+ from the cells
into the ECF may occur in patients with severe methabolic acidosis,
insulin deficiency (diabetes mellitus), rabdomyolisis. In the surgical
patients hyperkalemia occurs most frequently as a result of impaired renal
excretion of K+ caused by oliguric renal disfunction (therefore it should not
by added at the first postoperative 24h.
 The main risk that associated with hypernatremia are: weakness and
myocardial irritability. If untreated it can ultimately cause ventricular
fibrillation.
Treatment
 Individuals with mild hyperkalemia (less than 6mmol) can usually be
treated conservatively by reducing daily intake.
 - i.v. calcium gluconate (antagonizing effect);
 Depending on the cause: glucose, insulin, sodium bicarbonate
(translocation of potassium into cells), dialysis.

Calcium abnormalities
 99% of calcium is in bones. Within the ECF: free (40%) or bound to albumin (50%).
 May arise in patients with major fluid shifts, prolonged immobilization, alterations in GI
absorption or surgery on the thyroid or parathyroid glands.

Hypocalcemia
 Causes: acute pancreatitis, massive soft tissue infections, small-bowel fistulae, and
hypoparathyroidism.
 Earliest symptoms: numbness in the circumoral region or at the tips of the fingers. Tetany
or seizure may arise at more profound hypocalcemia.
 10ml ampoule of either 10% Ca gluconate or CaCl in 50-100ml D5W, or oral
supplementation may by sufficient.

Hypercalcemia
 Causes: primary hyperparatheroidism (malignancy).
 Symptoms may include confusion, lethargy, coma, muscle weakness, anorexia, nausea,
vomiting, pancreatitis or constipation.
 Most patients will respond to vigorous hydration. After rehydration, furosemide may be
administered to further increase calcium excretion. Treatment should by oriented on the
underlying cause.

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Acid-Base abnormalities

 The concentration of hydrogen ions: optimal pH range (7,35-7,45) to ensure

adequate function of proteins
proteins. This range is assured by the buffer systems
including intracellular proteins and phosphates and bicarbonat-carbonic
acid system. Further, alterations in excretion or retention of CO2 or HCO3
through changes in ventilation or renal tubular handling of HCO3 provide
an additional homeostatic mechanism for maintaining normal pH

 Arterial blood sample is recommended (venous value is lower, reflects

regional
g perfusion).
p ) Arterial blood sample
p should be transported
p on ice
quickly (RBC continue production of lactate - false high results)

 Acidemia (pH lower than 7.35);

 Alkalemia (pH higher than 7.35)

Methabolic acidosis.

At a pH below 7,2 catecholamine resistance develops such that the

myocardium and resistance vessels may not respond to either endogenous
or exogenous catecholamines.
catecholamines Loss of vasomotor tone and a reduction in
myocardial contractility may lead to cardiovascular collapse. The expected
compensation respiratory response is an increased ventilation to lower
carbon dioxide level.

Etiology
a)) retention ((or administration)) of fixed acids or
b) loss of bicarbonate.

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Lactic acidosis

 Inadequate tissue perfusion (hypovolemia) → aerobic metabolism is

inadequate triggering anaerobic metabolism → production and cumulation
of lactic acid.
 Restoration of tissue oxygenation helps to metabolize lactic acid by the
liver and kidneys resolving acidosis.
 If the perfusion is not restored and prolonged it may lead to irreversible
damage and cell death.
 All efforts should be oriented to restoration of perfusion. Oxygen delivery is
improved by increase of cardiac output (volume resus or sometime
inotropic agents), increase of [Hb] (RBC transfusion) if indicated.
Dichloracetate improves CO and oxidation processes - can be used.
 Restoration of perfusion and correction of underlying disorder. Correction
of IVV can be guided by simple UO measurement. At cardiac patients or
with renal insufficiency - CVP or PAWP to guide resus. In rare cases is
necessary to administer sodium bicarbonate parallel to fluid resus and
underlying disorder only if pH is below 7,2. (only in life-threatening
situations and judiciously).

Diabetic ketoacidosis

 Diabetus mellitus → insulin deficiency → impaired glucose utilization

→ energy deficit → liver produces ketones from free fatty acids to
supply alternative source of E → acetoacetic acid → B-hydroxybutyrate
→ aceton.
aceton Ketons are organic acids.
acids Especially it may be severe at
insulin-deficient patients with diabetes mellitus.
 Diagnosis: The nitroprusside test is used to measure keto acids in
blood and urine.
 Aim of treatment: correction of hypovolemia, hyperglicemia,
ketoacidosis, and K depletion (movement of potassium from the cells
into the ECV.
 Insulin is extrimely important,
important i.v.
i v bolus,
bolus subsequently by continuous
i.v. infusion.
 Fluid resus - control of hypovolemia (CVP to titrate volume repletion)
 Repletion of K under continuous ECG monitoring.

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Alcoholic ketoacidosis
 After sudden abstinence, one or three days after heavy drinking. commonly
associated with starvation or vomiting (volume depletion).
 Treatment: infusion therapy. D5W decreases keto acid formation in the
liver, saline promotes renal excretion of keto acid.
Acute and chronic renal failure
 Decreased excretion of acids, their cumulation.
Ingestion of toxins
1. Salicylate: accumulation of anions (salicylate).
 DS with chemical test for salicylate level.
 Treatment: adequate ventillation (sometime mechanical), correction of
fluid deficit, gastric lavage and administration of charcoal (minimize
absorption of drug from GIT). At some cases - dialysis.
2 Methanol
2. M h l and
d ethylene
h l glycol.
l l
 Is present in the antifreeze fluids and used as a cheap alternative to alc.
After ingestion are rapidly metabolized to toxic agents (formic acid and
glycolic acid)
 Treatment: gastric lavage and administration of charcoal. I.v. infusion of
ethanol (to inhibite metabolism of methanol of glycol. At some cases -
hemodialysis.

Rhabdomyoloisis
 Excessive muscle breakdown caused by myonecrosis. Accumulation of
organic acids and possible development of renal failure (block of renal
tubules).
 DS - level of myoHb
 Treatment: fluid resus agressive to prevent renal failure

Excessive bicarbonate loss

 From GIT losses (diarrhea, drainages, fistulas with loss of alkaly - billiary
and pancreatic secrets)
 Hypoaldesteronism and Addison's disease
Aldosteron deficit → reduction of acid secretion in the distal nephron
(defect of acidification)

Excessive acid administration

 Administration of large volume of blood preserved with citrate. Sometime
resus with huge volume of saline may cause it (so lactated Ringer's solution
(not so mach of Cl) is better to use).

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 22.07.2010

Diagnosis of metabolic acidosis

 arterial lactate concentration, serum and urine ketone

level, blood glucose level, serum [K], BUN, creatinine,
blood alcohol level. For rhabdomyolysis - urine
[myoglobin], methanol and ethylene glycol levels and
serum osmolality. They are necessary to determine the
cause off acidosis.
id i But
B if a patient
i iis obviously
b i l
underperfused and met acidosis improves with therapy,
further workup is not necessary.

Respiratory acidosis
Is caused by carbon dioxide retention due to inadequate alveolar ventilation
Hypoventilation → retention of CO2 → hypercapnea.
Compensation by renal bicarbonate (HCO3- ) retention (takes days).
Reduction in effective minute ventilation leads to an increase in PaCO2
and a reduction in HCO3.
 Common cause in postoperative patients is central respiratory depression
due to excessive postoperative sedation or narcotics (and CNS lesions).
 Other causes: airway obstruction: laringospasm requires dilators
(epinephrine, steroids, magnesium sulphate), removal of foreign bodies.
External compression by tumors, thyroid gland - usually surgical treatment
is indicated.
 pneumonia, pulmonary edema, ARDS, aspiration pneumonia.- treatment of
the cause.
 Respiratory muscle weakness: due to neuromuscular blocking agents;
neurologic diseases (multiple sclerosis, etc.)
 Depressed respiratory drive (depressing drugs, narcotics) - careful
administration.
 Treatment: improvement of ventilation, correction of the cause

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Methabolic alkalosis
Elevated plasma HCO3 concentration in the presence of arterial pH greater
than 7,45. The expected respiratory response is a reduction of minute
ventilation.
 Rare manifestations: neuromuscular excitability including paresthesias,
carpopedal spasm, or lightheadedness. There are three mechanisms of
elevation in plasma [HCO3]:
- loss of acids from GIT or urine;
- administration of HCO3, such as citrate (after massive blood transfusion);
- or loss of fluid with a high chloride/bicarbonate ratio;
 Vomiting results in both hypovolemia and loss of H+ and chloride.
Administration of NaCl replenish depleted Cl- levels and restore ECV.
 At life-threatening situations the acetazolamide should be considered
(i hibi off carbonic
(inhibitor b i anhydrase).
h d ) If iit iis not effective
ff i an exogenous acid
id
can be given (100 mEq/L of hydrochloric acid) via CV line. Under control
of arterial blood gases.
 Primary aldosteronism: the aldosteron excess acid secretion in the distal
nephron. Tratment is removal of source of mineralocorticoid excess. The
action of mineralocorticoid can be blocked by means of spironolactone or
amiloride.

Respiratory alkalosis

Is caused by increased loss of carbon dioxide due to hyperventilation.

 Respiratory alkalosis is common in surgical patients. Excessive pain, fever,
or gram-negative sepsis lead to an increase in central respiratory drive
causing in a reduction in PaCO2.
 DS: arterial blood gases show decreased PaCO2 and increased pH.
 pulmonary causes: diseases that affect the alveolar-capillary membrane
leading to ventilation-perfusion mismatch and finally to hypoxia. the body
responds by hyperventilation resulting in respiratory alkalosis (asthma,
pneumonia, congestive heart failure, pulmonary embolism, atelectasis,
pneumothorax.
pneumothorax
 If treatment is indicated, it should be directed toward the underlying cause.
Decrease ventilation (e.g., sedatives) or rebreathing the same air to
decrease carbon dioxide loss.
 If life-threatening it requires mechanical ventilation.

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