1. FLUID AND ELECTROLYTE
BALANCE
Dr Shermil Sayd
Dept of OMFS
KMCT dental college

2. Introduction
The prevention and treatment of fluid and
electrolyte disturbances are integral parts of
surgical care. To achieve homeostasis, the body
maintains strict control of water and electrolyte
distribution and of acid-base balance. This control
is a function of the complex interplay of cellular
membrane forces, specific organ activities and
systemic and local hormone actions.
Pestana C:fluids and electolytes in surgical patients, 2nd ed Baltimore, williams
and wilkins, 1981 pp 101-144

3. Total body water and composition
• Total body water accounts for 60% or more of
the body weight
• It varies according to the age, sex and
proportion of the body fat
• Water is contained mainly in the skeletal
muscle

4. FLUID COMPARTMENTS
• Two compartments
– Intracellular-approx two thirds of water
– Extracellular-rest one third of water

5. Extracellular water
– Interstitial water-75% of extracellular water
– Intravascular water- constitutes 25% of
extracellular water vol or 4% to 7%of body wt.
• They are separated by a semipermeable membrane
Volume (L)
% Total body
water
% Body weight
Plasma
3.5
8
4-7
Interstitium
10.5
25
15
Intracellular
28
67
40

6. Electrolytes and proteins in fluid compartments
• Balanced concentration of cations and anions
maintains electrical neutrality.
• In the intracellular compartment, potassium is
the dominant cation.
• In the interstitial and intravascular
compartments, sodium is the dominant
cation.

7. • Approximately 7%of plasma is in the form of
protein, mostly anionic albumin, which cannot
permeate the membrane.
• The distribution of ions across the
semipermeable membrane is called the
Donnan effect.
• The forces governing the distribution are
expressed as the Gibbs-Donnan equation

8. Osmolarity
• Prime determinants of water distribution in
the body.
• Refers to the number of particles dissolved in
a solution.
• In plasma, the major determinants of
osmolarity are sodium and its accompanying
anions, urea and glucose.

9. • Osmolarity expresses the concentration in
terms of osmoles of solute per liter of
solution.
• At the solute concentration of normal body
fluids, the osmolality and osmolarity are
nearly equivalent
• Gennari F:serum osmolality, N Engl J Med
310:102-105, 1984

10. Tonicity
• Determines the movement of water across the
cellular membrane.
• It is calculated by considering only the
concentration of the impermeable solutes in
the solution.
• Normal effective osmolarity of body fluids is
280 mOsm/kg

11. • A reduction in effective osmolarity implies a
relative water excess, whereas an increase in
effective osmolarity implies relative
dehydration

12. Regulation of volume
• Kidneys exert the greatest influence on the
regulation of intravascular volume.
• Osmoreceptors in the posterior pituitary
detect small changes in the serum osmolarity,
which then regulates the release of ADH.
• Baroreceptors in the kidney, carotid, and
elsewhere detect small changes in pressure

13. • Other key regulator is the Renin-AngiotensinAldosterone system.
• This leads to increase in the sodium
reabsorption and potassium excretion.

14. Fluid homeostasis
• Maintained under neuroendocrine and renal
control.
• Urinary losses of water are regulated by renal
mechanisms, with 300ml/day the minimal
volume required to allow solute excretion.
Along with this, insensible loss also occurs
through lungs and evaporative water loss
• Insensible loss increases by 10% for each 10C
increase in body temp

15. Volume excess
 Excess of water in the ECC w/ a normal
amount of solute or a deficient amount of
solute
 Occurs in prolonged and excessive diuresis,
forcing hypotonic fluids to produce diuresis
in the presence of renal impairment
 Fluid overload from production of adrenal
corticoid hormones [Cushing’s syndrome]

16.  Symptoms
 Weight gain & edema
 Cough, moist rales, dyspnea [fluid
congestion in lungs]
 CVP, bounding pulse,neck vein engorgement
[fluid excess in the vascular system]
 Bulging fontanelles
 Hg and Hct
 Nausea & vomiting

17.  Management
 Restrict fluids to lower fluid volume
 Diuretics or hypertonic saline
 Continuous assessments to prevent skin
breakdown
 Record daily weight to assess progress of
treatment

18. Volume deficits
• May occur from chronic or acute losses

19. Evaluation of chronic volume depletion
• Oliguria
• Loss of skin turgor
• Orthostatic hypotension
• Low urine sodium concentration
• BUN/creatinine ratio>15:1
• Hematocrit elevated by 5% or 6% per liter of
volume deficit

20. Evaluation of acute volume depletion
• Hypotension
• Tachycardia
• Tachypnea
• End-organ hypo-perfusion
• Skin mottling
• Acidosis

21. Treatment
• An isotonic solution, such as lactated ringers
solution is highly effective in restoring
circulating volume.
• Normal 0.9% NaCl saline solution is commonly
used
• Calcium, magnesium, and phosphorous
supplements are not required for short-term
therapy unless critically ill.

22. • If the patient is febrile maintenance fluid must
be increased by 10%for each degree above
37.20C

23. IV fluid composition
Solution
Na+
K+
Ca+
Mg+
Cl-
HCO3
Glu
Osm
0.9%NaCl(NS)
154
-
-
-
154
-
-
308
D5/0.9%NaCl
154
-
-
-
154
-
50
560
0.45%NaCl(1/2NS)
77
-
-
-
77
-
-
560
D5/0.45% NaCl
77
-
-
-
77
-
50
406
0.225% NaCl(1/4)
38.5
-
-
-
38.5
-
-
77
D5/0.225% NaCl
38.5
-
-
-
38.5
-
50
329
LR
130
4
3
-
109
28
-
273
3.0% NaCl(hypertonic)
513
-
-
-
513
-
-
1026

24. SODIUM HOMEOSTASIS
• Normal dietary intake is 6-15g/day.
• Sodium is excreted in urine, stool, and sweat.
• Urinary losses are tightly regulated by renal
mechanisms.

25. Sodium abnormalities
Hypernatremia:
• Defined as a serum sodium concentration that
exceeds 150mEq/L.
• Always accompanied by hyperosmolarity

26. Etiology
• Excessive salt intake
• Excessive water loss
• Reduced salt excretion
• Reduced water intake
• Administration of loop diuretics
• Gastrointestinal losses

27. Evaluation
• With history, physical examination and
assessment of volume status
• Very young and the very old and the
debilitated are more susceptible
• Symptoms:
malaise, lethargy, vomiting, generalized
seizures and coma

28. • Most severe cases : bridging intracranial
vessels rupture, causing intracerebral and
pericerebral hemorrhage
• In chronic hypernatremia, more time is
available for cerebral adaptation by the
intracellular accumulation of organic
osmolites, called as cerebral osmoregulation.
The brain is the only organ with this potential.

29. Treatment:
• Restore circulating volume with isotonic saline
solution
• After intravascular vol. correction
hypernatremia is corrected using free water in
the form of D5W.
• The free water deficit can be calculated as the
difference between NTBW and CTBW.

30. Hyponatremia
• Serum sodium concentration less than
135mEq/L

31. Etiology
• Excessive water intake
• Impaired renal water excretion
• Loss of renal diluting capacity

32. Symptoms:
• Mostly neurologic and due to cellular swelling
induced by ECF hypo-osmolality
• Cerebral swelling leads to lethargy, confusion,
vomiting, seizures and coma
• Symptoms rarely occur until serum sodium
concentration goes below 120mEq/L
• Severity related to rate of decrease

33. Classification:
• Hypervolemic
• Normovolemic
• Hypovolemic
• Pseudohyponatremia

34. Hypervolemic
• Have edema
• Cause: renal failure, CHF, COPD with
hypercarbia, and severe liver disease

35. Normovolemic :
• Cause: Syndrome of Inappropriate secretion of
ADH(SIADH)
• SIADH is seen in patients with stroke or injury
and in pulmonary conditions such as
tuberculosis and cancer
• Plasma vol. is normal or slightly elevated

36. Hypovolemic
• Have renal or extrarenal loss of sodium
greater than that of the water losses.
• Urinary sodium level
– >20mEq/L-renal loss associated with diuretic
use, aldosterone deficiency, salt losing
nephritis, renal failure and subarachnoid
hemorrhage.
– <10mEq/L- normal tubular response to
hyponatremia

37. • Extra renal loss occurs as vomiting, fistula or
diarrheal loss

38. Pseudohyponatremia
• Two situation
– in hyperlipidemia or hyperproteinemia
– Osmotically active glucose
• 100 mg/dl increase in the serum glucose will suppress
serum sodium by 1.6mEq/L

39. Treatment :
• Hypervolemia- volume restriction and loop
diuretics. In patients with renal failure, dialysis
might be required.
• SIADH patients usually responds to fluid
restriction
• Hypovolemia- salt and water replacement
• If due to endocrine deficiencies, hormonal
replacement indicated

40. • Asymptomatic- should be treated slowly.
Isotonic saline preferred. Addition of loop
diuretics will hasten water excretion, provided
plasma volume is restored
• Fluid restriction, loop diuretic and correction
of the underlying cause is sufficient in
normovolemic or hypervolemic states

41. • Symptomatic- associated with seizures or coma.
Danger of neurologic damage exists if sodium
level increased rapidly. Central pontine myelinosis
has been shown to occur in rapid correction of
hyponatremia.
• Current recommendation is, no faster than
0.5mEq/L/hr.
• A concentration of 120mEq/L is sufficient. After
the symptoms have abated, sodium correction
should occur at a still slower rate.

42. • Total sodium deficit(TSD):
TSD=0.6XWEIGHT IN KG X (140-MEASURED Na+)
• In patients with stupor and coma, hypertonic
saline(3%NaCl) solution is used. Objective is to
restore sodium rapidly to 120mEq/L, at a correction
no greater than 0.5mEq/L/hr. thereafter correction
may be at a slower pace with isotonic saline.
Oh M, Corrol H: disorders of sodium metabolism:
hypernatremia and hyponatremia. Crit care Med 20:94103, 1992

43. Potassium homeostasis
• Principal intracellular cation in the body
• Quantity in avg. sized adult is 3800mEq/L or
55mEq/Kg.
• Located mostly in the skeletal muscle
• Paramount for the function of excitable tissue.
• Normal plasma conc. Is 3.5 to 5mEq/L.
• Internal factors responsible for the maintenance
include insulin, aldosterone, catecholamine and
acid base balance

44. Potassium abnormalities
Hyperkalemia
• Serum potassium > 5.5mEq/L

45. Etiology
• Renal or adrenal insufficiency
• Metabolic acidosis
• Iatrogenic causes
– Medications(NSAID, ACE inhibitors)
– Excessive administration of potassium
•
•
•
•
Intravascular hemolysis
Rhabdomyolysis
Seizures
Severe GI bleeding

46. Pseudohyperkalemia:
• In vitro hemolysis due to excessive agitation of
the sample before reaching the lab.
• Prolonged tourniquet time and fist clenching
during blood draw(increase by 1.6mEq/L)
• Thrombocytosis and leukocytosis
• True K levels are measured using plasma

47. Evaluation:
• Myocardial effects
– Conc. Increase to 6mEq/L
• Peaking of the T-wave
• Prolonged PR interval
• RR interval increases
– Above 6mEq/L
• Loss of P waves
• Widening of the QRS complex

48. – Final outcome
• Complete heart block
• Ventricular tachycardia
• Cardiac standstill
• Extracardiac symptoms
– Paresthesias
– Flaccid paralysis
– ileus

49. Treatment:
• Reversal of cardiac toxicity
• 10-20ml 10% calcium gluconate should be
administered. Action starts in 1-5mins and
lasts for 30mins.
• Concurrent treatment with insulin or sodium
bicarbonate moves the potassium into the
cells

50. • Administering 10unts of insulin in5oml of a
50% dextrose solution will elicit a response in
15 to 45mins and lasts for 4-6 hrs
• K can be removed from the body by
– Cation exchange resin kayexalate (50-100mg) as
enema
– 40gm orally with sorbitol, each gm removes
approx. 0.5 to 1mEq of K. onset of action os slow
and lasts for 4-6hrs
– Effective method-dialysis

51. Hypokalemia:
• Serum potassium level<3.5mEq/L

52. Etiology:
• GI losses from vomiting, diarrhea, or fistula
and use of diuretics

53. Evaluation:
• Metabolic alkalosis often co-exists with
hypokalemia, decreases serum K level.
• Generalized weakness and fatigue
• ECG
– Flattened T-wave
– Diminished QRS voltage and U waves
In digoxin taking patients hypokalemia will cause
life threatening arrhythmias

54. Treatment:
• Correction of the underlying condition
• K should be given orally unless
severe(<2.5mEq/L), patient is symptomatic or
the enteral route is contraindicated
• Oral K supplements (60-80mEq/L) coupled
with normal diet is sufficient.
• ECG monitoring along with frequent
assessment of serum K level is reqiured

55. Calcium homeostasis
• Body contains approx. 1400gm of calcium
• Reduction in calcium level leads to PTH
secretion which increases calcium
reabsorption from the bone. It increases
calcium reabsorption from the DCT and
stimulates the formation of the active
metabolite of vit. D that increases gut
reabsorption of elemental calcium and
facilitates the PTH action on the bone

56. Calcium abnormalities:
Hypercalcemia:
• Ionized calcium conc. > 5.3mg/dL

57. Etiology:
• Hyperparathyroidism
• Cancer
• Paget's disease
• Pheochromacytoma
• Hyperthyroidism
• Thiazide diuretics

58. Evaluation:
• Moderate hypercalcemia(5.3-6.5mg/dL) tend to
be asymptomatic or complain only of malaise
• Severe hypercalcemia– Neurologic symptoms
• Lethargy->stupor and coma
– CV manifestation
• Arrythmia
• Shortened QT interval

59. – GI effects
•
•
•
•
Anorexia
Constipation
Pancreatitis
Hyperacidity
– Renal defect
• Polyuria

60. Treatment:
• Severe hypercalcemia– If hyperparathyroidism-surgery
– Initial supportive therapy includes furosamide to
increase calcium excretion
• Calcitonin reduces bone resorption and has an
immediate effect and lasts for 48 hrs.
prolongation can be done by using
corticosteroids

61. • Bisphosphonates are effective in inhibition of
osteoclastic activity, but onset of action is very
slow( 2-3 days)
• Mithramycin has rapid onset of action, but is
associated with renal and hepatic toxicity.
• Dialysis is required in patients with renal
failure

62. Hypocalcemia:
• Ionized calcium conc. < 4.4mg/dL

63. Etiology:
• Parathyroid or thyroid surgery
– onset immediate(hrs) or delayed(1-2 days)
• Severe pancreatitis
• Magnesium deficiency
• Massive blood transfusion

64. Evaluation:
• Mild or moderate
– Asymptomatic
• Severe
– Neuromuscular
•
•
•
•
•
Paresthesia
Muscular spasm
Seizures
Tetany
weakness

65. • Laryngospasm
• Bronchospasm
• Chvostek sign
– CV symptoms
•
•
•
•
•
Arrythmias
Heartblock
Bradycardia
Refractory hypotension
ECG- prolongation of the QT interval and T-wave
inversion

66. Treatment:
• Treatment of the underlying disorder
• Asymptomatic
– Calcium supplementation is not required
• Symptomatic
– IV calcium therapy- initially 100mg elemental
calcium over a period of 5-10mins.susequently, a
calcium infusion of 0.5-2mg/kg/hr is given

67. • Once calcium conc. is corrected, enteral therapy
with elemental calcium is begun at a dosage of 14gm/day
Kobrin S, goldfarb s: hypocalcemia and
hypercalcemia. In adrogue H acid base and
electrolyte disorders.
Newyork, churchill, livingstone, 1991, pp69-96

68. Magnesium homeostasis
• 2nd most plentiful intracellular cation
• Adult body contain 2000mEq of
magnesium(Mg)
• Normal concentration range 1.6 mEq to
2.1mEq/L
• Daily consumption-25 mEq
• Excretion- one third by stool and the rest by
renal excretion

69. Magnesium abnormalities:
Hypermagnesemia:
• Serum magnesium level >2.1 mEq/L

70. Etiology:
• Decreased GFR
• Addison’s disease

71. Evaluation:
• Symptomatic when serum Mg>4 mEq/L
• Neuromuscular sequelae
– Loss of deep tendon reflex
– Somnolence
– Apnea
• Cardiac effects
– Bradycardia
– Heart block
– Cardiac arrest( extreme elevation)

72. Treatment:
• Symptomatic– Antagonizing using calcium infusion(5-10 mEq )
– Followed by immediate dialysis
– If renal function normal, saline diuresis
• Long term therapy- remove all exogenous Mg
intake

73. Hypomagnesemia:
• Serum Mg concentration<1.6 mEq/L

74. Etiology:
• GI losses
• Reduced absorption(short bowel syndrome)
• Excessive urinary losses
– Alcoholism
– 10 aldosteronism
– Diuretics

75. Evaluation:
• Neuromuscular effects
– Tremor
– Ataxia
– Carpopedal spasm
– Tetany
• Cardiotoxicity
– Prolonged QT interval->ventricular tachycardia

76. Treatment:
• Symptomatic
– Mg infusion(8-16 mEq over a 5-10 min
period, followed by 48 mEq/day)
• If asymptomatic- Mg supplements given orally

77. Phosphate homeostasis
•
•
•
•
Dietary intake-800-1200mg/day
Reabsorbed in the jejunum
Kidney acts as the principle regulator
Normal serum P conc. Is 2.5-4.5mg/dL

78. Phosphate abnormalities:
Hyperphosphatemia:
• Serum phosphate level>4.5mg/dL

79. Etiology:
• Renal insufficiency
• Thyrotoxicosis
• Malignant hyperthermia
• Hypoparathyroidism

80. Evaluation:
• Few symptoms associated
• Commonly discovered by lab testing
• Chronic hyperphosphatemia leads to
metastatic calcifications and arterial
obstruction(calciphylaxis)

81. Treatment:
• Treatment of the underlying renal failure
• Chronic- phosphate binding antacids are
effective
• Acute- end stage renal disease. Dialysis is
required

82. Hypophosphatemia:
Serum phosphate level <2.5mg/dL

83. ETIOLOGY:
• Transcellular shifts
• excessive urinary losses
• Decreased dietary intake
• Decreased intestine absorption
• Diuretics
• Hyperparathyroidism
• Malabsorption
• Hypomagnesemia
• Vit. D deficiency

84. • Severe hypophosphatemia
– Chronic respiratory alkalosis
– Chronic alcoholism
– Severe burns
– Treatment of diabetic ketoacidosis

85. Evaluation:
• Mild/moderate reduction- no signs
• Severe hypophosphatemia
– Myalgias
– Muscle weakness
– CHF
– Respiratory insufficiency

86. Treatment:
• Oral or parenteral phosphate repletion and
correction of the underlying disorders

87. Electrolyte Disorders
Signs and Symptoms
Electrolyte
Excess
Deficit
Sodium (Na)
•Hypernatremia
•Thirst
•CNS deterioration
•Increased interstitial fluid
•Hyponatremia
•CNS deterioration
Potassium (K)
•Hyperkalemia
•Ventricular fibrillation
•ECG changes
•CNS changes
•Hypokalemia
•Bradycardia
•ECG changes
•CNS changes

88. Electrolyte Disorders
Signs and Symptoms
Electrolyte
Excess
Deficit
Calcium (Ca)
•Hypercalcemia
•Thirst
•CNS deterioration
•Increased interstitial fluid
•Hypocalcemia
•Tetany
•Chvostek’s, Trousseau’s
• Hypermagnesemia
• Loss of deep tendon
•Hypomagnesemia
•Hyperactive DTRs
•CNS changes
Magnesium (Mg)
reflexes (DTRs)
• Depression of CNS
• Depression of
neuromuscular function
signs
•Muscle twitching
•CNS changes
•ECG changes

89. Acid-Base Balance
• Usually present clinically as
– Tissue malfunction due to disturbed pH
– 20 changes in respiration as a response to the
underlying metabolic changes.
• Clinical picture is dominated by the cause of the
acid-base change, such as uncontrolled diabetes
mellitus or primary lung disease
• Only becomes evident when the venous plasma
bicarbonate conc. Is noted to be abnormal, or
when a full arterial blood gas analysis shows
abnormalities in the pH, PCO2 or bicarbonate

90. • In metabolic disturbances, respiratory
compensation is almost immediate to achieve
the predicted PCO2 immediately after the
onset of the metabolic disturbance.

91. Metabolic Acidosis
Etiology and assessment
• Occurs when acids other than carbonic acid
accumulates in the body resulting in ↓
plasma bicarbonate

92. Causes of metabolic acidosis
Disorder
A. Normal anion gap
• Inorganic acid addition
•
GI base loss
•
Renal tubular acidosis
B. Increased anion gap
Endogenous acid load
Diabetic ketoacidosis
Starvation ketosis
Lactic acidosis
Renal failure
Exogenous acid load
Aspirin poisoning
Methanol poisoning
Ethylene glycol poisoning
Mechanism
-Therapeutic infusion of or poisoning with NH4Cl,
HCl
-Loss of HCO3 in diarrhea, small bowel fistula,
urinary diversion procedure.
-Urinary loss of HCO3 in proximal RTA; impaired
tubular acid secretion in distal RTA
-Accumulation of ketones with hyperglycemia
-Accumulation of ketones without hyperglycemia
-Tissue hypoxia or liver disease
-Accumulation of organic acids
-Accumulation of salicylate
-Accumulation of formate
-Accumulation of glycolate, oxalate

93. • Two patterns are seen
– Pattern A-when a mineral acid accumulates or
when there is a primary loss of bicarbonate buffer
from the ECF, there is no addition of the acidic
anion. In this case anion gap occurs, which is
normal, since the plasma chloride increases to
replace the depleted bicarbonate levels.
– Usually occurs due to diarrhea, where the clinical
generally obvious or to RTA.

94. – Pattern B- accumulating acid is accompanied by its
corresponding anion, which adds to the
unmeasured anion gap, while the chloride level
remains normal.
– Cause is usually apparent from the clinical signs
such as diabetes mellitus, renal failure or shock.
– Other causes include alcoholism, starvation
ketosis, lactic acidosis and intoxication by
methanol

95. Management:
• Identify and correct the cause
• IV fluid resuscitation is needed due to associated water and
sodium depletion
• Bicarbonate infusions can be started in cases where the
underlying cause cannot be identified and the acidosis level is
critical(H+ >100nmol/L, pH < 7).

96. Metabolic alkalosis
• It’s the inability of the kidney to excrete the
excess bicarbonate ions or to retain hygrogen
ion.
• Usually accompanied by respiratory
compensation
• PCO2 increases 5-7mmHg for each 10 mEq/L
of increase in plasma concentration.

97. Etiology:
• Two types
– Chloride responsive metabolic alkalosis
• Have contracted ECF vol. and chloride deficit and
urinary chloride<10 mEq/L
• Vomiting and high nasogastric output are the common
causes
• Deficit chloride gap is filled by bicarbonate
• In late stages, H is exchanged for Na.

98. – Chloride-unresponsive metabolic alkalosis
• Are normovolemic or hypovolemic
• Urinary chloride conc. >10 mEq/L.
• E.g.:- cushing’s syndrome
• High metabolic alkalosis is associated with a
cerebral hypoperfusion, a leftward shift of the
oxyhemoglobin dissociation curve and
hypokalemia

99. Treatment:
• Correction of the underlying defect
• Contraction alkalosis treated with saline
• With chloride unresponsive metabolic alkalosiscarbonic anhydrase inhibitor, acetazolamide.
• Severe alkalemia treated with an infusion of 0.1N
HCl.
• The source of mineralocorticoid, if possible,
should be corrected

100. Respiratory acidosis
• Present when the pH is low and the PCO2 is
elevated
• Two types based upon etiology, time of
evolution of the disorder and the degree of
renal compensation
– Acute
– Chronic

101. Etiology :
• Due to ineffective alveolar ventilation
• Decompensation of pre existing respiratory
disease
• Asthma
• Neuromuscular disorders
• CNS depression
• Airway obstruction

102. Evaluation:
• In acute, resp. acidosis, the expected response is
only 1 mEq increase in HCO3- for each 10 mm Hg
rise in PCO2
• In chronic respiratory acidosis, renal adaptation is
substantial
• Plasma bicarbonate concentration increases 3 to
4 mEq/L for each 10mm Hg rise in PCO2
• Renal compensation never restores the pH to the
normal levels

103. Treatment:
• Improve alveolar ventilation
– By intubation
– By mechanical ventilation
• Chronic respiratory acidosis the goal is the
restoration of a compensated steady state
because the underlying defect is usually
uncorrectable

104. Respiratory alkalosis
• Present when the pH is high and PCO2 is low
• May be acute or chronic

105. Etiology:
• Alveolar hyperventilation
• In surgical patients
– Hypoxia
– CNS lesions
– Pain
– Hepatic encephalopathy
– Mechanical ventilation

106. Evaluation:
• In acute respiratory alkalosis(ARA), renal
compensation is minimal.
• In chronic respiratory alkalosis(CRA) , kidney
responds by decreasing the excretion of the
hydrogen ion
• Serum bicarbonate conc. Is expected to decrease
by 4-5 mEq/L for each 10mm Hg decrease in the
PCO2
• Usually patient asymptomatic

107. • Severe alkalosis may have carpopedal spasm,
circumoral numbness, cramps and confusional
states.
• Hyperventilation is particularly dangerous in
patients with subarachnoid hemorrhage
because it exacerbates vasospasm

108. Treatment:
• Correction of the underlying problem.

109. Summary
• Fluid compartments in the body must balance
• Body systems regulate F&E balance
• Assessment of body fluid is important to
determine causes of imbalance
• Interventions for imbalances are based on the
cause

110. References
• Oral and maxillofacial surgery-Daniel M Laskin
• Essentials of surgery-Becker and Stucchi
• Adrogue H, madias N: management of life
threatening acid base disorders. N Engl J Med
338:26-34, 1998
• Gennari F:serum osmolality, N Engl J Med
310:102-105, 1984
• Kobrin S, goldfarb s: hypocalcemia and
hypercalcemia. In adrogue H acid base and
electrolyte disorders. Newyork, churchill,
livingstone, 1991, pp69-96

111. • Oh M, Corrol H: disorders of sodium
metabolism: hypernatremia and
hyponatremia. Crit care Med 20:94-103, 1992
• Pestana C:fluids and electolytes in surgical
patients, 2nd ed Baltimore, williams and
wilkins, 1981 pp 101-144