FLUID VOLUME EXCESS

Anis Ashraf
Lecturer
LEARNING OBJECTIVES

By the end of the session learners will be able

to:
 Discuss the causes, pathophysiology and
manifestation of the following Fluid volume
Excess
 Discuss Assessment and Diagnostic Test,
Medical and Nursing Management of Fluid
volume Excess

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 FLUID VOLUME EXCESS
(HYPERVOLEMIA)
• Fluid volume excess (FVE) refers to an isotonic
expansion of the ECF caused by the abnormal
retention of water and sodium in approximately the
same proportions in which they normally exist in the
ECF.
• It is always secondary to an increase in the total body
sodium content, which, in turn, leads to an increase
in total body water.
• Because there is isotonic retention of body
substances, the serum sodium concentration remains
essentially normal.
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 FLUID VOLUME EXCESS
• Extracellular: Intracellular:
Isotonic fluid excess.
water excess
 Excess of body
• Excess of both water
and electrolytes water without excess
electrolytes
• Caused by retention  Caused by over-
of water and hydration in the
electrolytes related to presence of renal
kidney disease;
overload with failure; administration
isotonic IV fluids of D5W

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 PATHOPHYSIOLOGY
• FVE may be related to simple fluid overload or diminished
function of the homeostatic mechanisms responsible for
regulating fluid balance.
• Contributing factors can include:
– heart failure,
– renal failure, and
– cirrhosis of the liver.

Another contributing factor is

• Consumption of excessive amounts of table or other sodium
salts.
• Excessive administration of sodium-containing fluids in a patient
with impaired regulatory mechanisms may predispose him or her
to a serious FVE as well

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 CLINICAL MANIFESTATIONS
Clinical manifestations of FVE stem from expansion of the
ECF and include:
–Edema,
–Distended neck veins, and
–Crackles (abnormal lung sounds).
Other manifestations include:
–Tachycardia;
–Increased blood pressure,
–Pulse pressure, and
–Central venous pressure;
–Increased weight;
–Increased urine output;
–Shortness of breath and
–Wheezing.

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• Laboratory data useful in diagnosing FVE
include:
– BUN and hematocrit levels.
– In FVE, both of these values may be decreased
because of plasma dilution.
• Other causes for abnormalities in these values
include:
– low protein intake and anemia.
• In chronic renal failure, both serum
osmolality and the sodium level are decreased
due to excessive retention of water.

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 Cont.

• The urine sodium level is increased if the

kidneys are attempting to excrete excess
volume.
• Chest x-rays may reveal pulmonary congestion.
• Hypervolemia occurs when aldosterone is
chronically stimulated (ie, cirrhosis, heart
failure, and nephrotic syndrome).
• Urine sodium levels, therefore, will not rise in
these conditions.

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 MEDICAL MANAGEMENT
• Management of FVE is directed at the causes.
When the fluid excess is related to excessive
administration of sodium-containing fluids,
discontinuing the infusion may be all that is
needed.
• Symptomatic treatment consists of
administering diuretics and restricting fluids
and sodium.

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 FLUID VOLUME EXCESS/ Treatment
• Isotonic  Hypotonic

– Correct cause  Correct cause

– Restrict H2O  Restrict H2O intake

and Na  IV fluids with E-lytes
– Diuretics
– Digitalis
– Possible dialysis

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 NURSING INTERVENTIONS
• Daily weight
• Intake and output
• High Fowler’s position.
• Bed rest favors diuresis
• Assess breath sounds
• Monitor edema with millimeter tape
• Monitor venous distention
• Sodium restricted diet
• Skin care and turn frequently

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• Elevate edematous extremities, and handle with care
• Take diuretics as prescribed.
• Consider interventions related to specific etiological
factors (e.g., inotropic medications for heart failure,
paracentesis for liver disease).
•  Avoid foods that are enjoyable, canned, and frozen
foods.
• Cook without salt, and use spices to add flavor
(lemon, basil, mint)
• Use vinegar salt substitute to taste soup, stew, etc.

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 REFERENCE

Brunner, L. S. (2010). Brunner & Suddarth's textbook

of medical-surgical nursing (Vol. 1). S. C. C.
Smeltzer, B. G. Bare, J. L. Hinkle, & K. H. Cheever
(Eds.). Lippincott Williams & Wilkins.

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