This document discusses disorders of fluid and electrolyte imbalances. It covers isotonic imbalances like hypovolemia and hypervolemia, osmotic imbalances like hyponatremia and hypernatremia, and compositional imbalances like hypokalemia and hyperkalemia. It describes the causes, clinical manifestations, pathophysiology, diagnostic evaluations, and treatment of each of these conditions. It also discusses fluid distribution in the body, fluid movement between plasma and tissues, and edema.

1. DISORDERS OF FLUID, ELECTROLYTES
IMBALANCE

2. OBJECTIVES
At the end of this presentation, the student will be able to;
 Discuss the causes, clinical manifestation, and pathophysiology of following
Isotonic imbalance:
1. Hypovolemia.
2. Hypervolemia.
 Discuss the causes, clinical manifestation, and pathophysiology of following
Osmotic imbalance
1. Hyponateremia.
2. Hypernateremia.

3. CONT…
 Discuss the causes, clinical manifestation, and pathophysiology of following
Compositional Imbalance:
1. Hypokalemia.
2. Hyperkalemia.

4. FLUID DISTRIBUTION
 Intracellular Fluid Compartment:
Fluid inside the cells cytoplasm or membranes
 Extracellular Fluid Compartment:
o Interstitial (tissue) spaces.
o Plasma (vascular) compartment
o Transcellular compartment
• Cerebrospinal fluid
o Cavities:
peritoneal (gut), pleural (lungs), pericardial (heart), joints (synovial)

5. DISTRIBUTION WATER IN THE BODY
 Water is 60% of body weight in a healthy male 50% in a healthy female.
 75% to 80% in infants.
 Total body water decreases with ageing.
o Increased Adipose tissues due to fats accumulation.
o Decreased muscle mass.
o Renal Decline due to which more water lost in urine.
o Diminished thirst perception.
 About 2/3 of the body fluid content is present intracellular.
 About `1/3 of the body fluid content is present extracellular (plasma water
and interstitial water).
 Transcellular compartments usually contain less than 1% .

7. FORCES MOVE IN AND OUT OF CAPILLARIES
 Hydrostatic Pressure (push):
o This is the pressure exerted by a
fluid, e.g. blood
o The hydrostatic pressure in this
example is the blood pressure,
generated by the contraction of the
heart muscle
o Capillary filtration pressure –pushes
water out through
aquaporin's(water pores).
o Pressure in the interstitial fluid
resists-essentially pushing back.
o Normally water flows out of the
capillary.

8. CONT…
 Colloidal Osmotic/Oncotic pressure
(pull):
o This is the osmotic pressure exerted
by plasma proteins within a blood
vessel
o Plasma proteins lower the water
potential within the blood vessel,
causing water to move into the
blood vessel by osmosis
o Solutes “pull” water from both the
capillary and the interstitial fluid.
o Normally more water is pulled into
the capillary unless there is a
buildup of proteins or other
particles in the interstitial fluid.

9.  At the arterial end:
o When blood is at the arterial end of
a capillary the hydrostatic
pressure is great enough to force
fluid out of the capillary
o Proteins remain in the blood as
they are too large to pass through
the pores in the capillary wall
o The increased protein
content creates a water
potential gradient (osmotic
pressure) between the capillary
and the tissue fluid
o At the arterial end the hydrostatic
pressure is greater than the
osmotic pressure so the net
movement of water is out of the
capillaries into the tissue fluid.
 At the venous end:
o At the venous end of the capillary
the hydrostatic pressure within the
capillary is reduced due to
increased distance from the heart
and the slowing of blood flow as it
passes through the capillaries
o The water potential
gradient between the capillary and
the tissue fluid remains
the same as at the arterial end
o At the venous end the osmotic
pressure is greater than the
hydrostatic pressure and water
begins to flow back into the
capillary from the tissues fluid

10. CONT…
o Roughly 90 % of the fluid lost at the arterial end of the capillary is
reabsorbed at the venous end
o The other 10 % remains as tissue fluid and is eventually collected
by lymph vessels and returned to the circulatory system
o If blood pressure is high (hypertension) then the pressure at the arterial
end is even greater
o This pushes more fluid out of the capillary and fluid begins to accumulate
around the tissues. This is called Edema.

11. FLUID MOVEMENT BETWEEN PLASMA AND
INTERSTITIAL SPACE

12. EDEMA
 Accumulation of fluid within the interstitial spaces
 Edema may be of two types:
1. Pitting edema:
When pressure is applied to the skin of the swollen area
and released back an indentation is left behind (e.g. when skin is pressed
with a finger or when stockings or socks induce indentation.
o Pitting edema indicates that fluid flow to the area is somehow restricted
(trouble refilling
1. non-pitting edema:
may indicates fluid is not being drained properly,
mostly protein rich fluid is present in interstitial spaces.( lymphedema due
to blockage of lymph nodes)

13. SOME COMMON CAUSES OF EDEMA
 Increased capillary Hydrostatic pressure:
Increased vascular volume ( more blood in vessels) ,Heart failure or kidney disease
may lead to increased fluid retention.
Venous obstruction (blood clot lodged in a vein thrombophlebitis.
 Decreased plasma colloidal oncotic (osmotic) pressure:
kidneys disease may lead to protein loss into urine (less in capillaries)
Liver disease may cause less protein secretion into blood (also malnutrition)
 Increased capillary permeability:
Inflammation, Allergic reactions, capillary damage from malignancy, tissue injury or
burns.
 Obstruction of Lymphatic ducts:
Malignancy or removal of lymph nodes.

14. FLUID VOLUME DEFICIT( HYPOVOLEMIA)
 Definition:
Hypovolemia is defined as the condition that occurs when loss of
extracellular fluid volume exceeds the intake of fluid.
o Both fluids and electrolytes are lost together in isotonic fashion.
o Other names FVD, hypovolemia, volume depletion, volume contraction or
oligemia.
 Extracellular fluid:
o Fluid outside the cells. It contains sodium, chloride, bicarbonates ions,
oxygen, carbon dioxide, glucose, fatty acids and amino acids plus cellular
wastes.
o ECF:
Interstitial fluid, intravascular fluid and transcellular fluid.

15. CAUSES AND RISK FACTORS
FVD results from the loss of body fluids and occurs more rapidly when coupled
with decrease fluid intake. Obvious causes of hypovolemia includes:
 Abnormal fluid losses
such as those resulting
from:
o Traumatic accidents
o Extensive vomiting
o Sever Diarrhea
o GI Suctioning
o Profuse Sweating
o Internal bleeding and
Dehydration
o Ruptured ectopic
pregnancy
o Drainage from wounds
or fistula
o Burns and Diuretic
therapy
 And decreased intake
as in:
o Nausea
o Poor intake of fluids
o Long term NPO
o Fever
 Additional Risk factors:
o Diabetes insipidus
o Adrenal insufficiency
o Osmotic diuresis
o Hemorrhage
o coma

16. COMPLICATION
 When someone losses about 20% (1/5) of blood volume, anyone can enter to
such type of circumstances called hypovolemic shock.
 Hypovolemic shock:
Hypovolemic shock is a life-threatening condition during
which organs learn to fail due to reduced blood and oxygen supply.

17. PATHOPHYSIOLOGY
 Decreased circulating volume and a subsequent reduction in the amount of
blood reaching the tissues of the body.
 In order to properly perform their functions, tissues require oxygen
transported through blood.
 A decrease in circulating volume can lead to decrease in blood flow to the
brain, resulting in headache and dizziness.
 Baroreceptors in the body sense the reduction of circulating fluid and send
signals to the brain to increase sympathetic response.

18. CONT…
 Sympathetic response is to release epinephrine and norepinephrine, which
results in peripheral vasoconstriction, in order to conserve the circulating
fluid for vital organs to survive.
 Peripheral vasoconstriction accounts for cold extremities, increased heart
rate, increased cardiac output.
 Eventually, less perfusion to the kidneys, resulting in oliguria.

19. CLINICAL MANIFESTATION
FVD can develop rapidly and can be mild, moderate, or sever depending on the degree of
fluid loss.
o Thirst
o Weight loss
o Cyanosis
o Poor skin turgor
o Dry skin and dry mouth
o Low blood pressure
o Increased body
temperature
o Decreased urine output
(oliguria)(400-
500ml/day)
o Concentrated urine
o Change in mental
status
o Muscle weakness and
cramps
o Postural hypotension
o Weakness and rapid
heart rate
(tachycardia)
o Chest pain
o Decreased central
venous pressure
o Headache
o Dizziness
o Cool, clammy skin
o Sunken eyes
o Dry eye
o Restlessness

20. ASSESSMENT AND DIAGNOSTIC FINDINGS
 Elevated blood urea nitrogen (BUN) level (greater than 25mg/dl.
 Elevated hematocrit level (greater than 55%)
 Specific gravity of urine also increases (greater than 1.030)
 Hypokalemia occurs with GI and Renal losses.
 Hyperkalemia occurs with adrenal insufficiency.
 Hyponatremia occurs with increasing thirst and ADH release.
 Hypernatremia results from increased insensible losses and diabetes insipidus.

21. MEDICAL MANAGEMENT
 Emergency resuscitation to assure adequate tissue perfusion.
 History to detect cause of hypovolemia.
 Physical exam to confirm hypovolemia and to assess severity.
 MILD: oral fluids will given to treat hypovolemia.
 MODERATE TO SEVERE: IV therapy is used.
 Electrolytes solution (e.g. lactated Ringer’s ), 500ml to 1000ml normal saline .

23. HYPERVOLEMIA
 It is also called fluid volume excess.
 DEFINITION:
Hypervolemia or fluid overload or over hydration is the medical
condition where there is too much fluid in the body.
o 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 in
total body water.

24. CAUSES
o Excessive intake of sodium
containing fluids
o Excessive salt intake
o Excessive sodium bicarbonate
therapy
o Congestive heart failure
o Renal failure
o Cirrhosis of liver
o Primary polydipsia
o Cushing syndrome
o Long term use of corticosteroids
o Fluid remobilization after burn
treatement

25. PATHOPHYSIOLOGY
 Contributing factors can include heart failure, renal failure, and cirrhosis of
the liver.
 Another contributing factor is consumption of excessive amount of table or
sodium salts.
 Excessive administration of sodium-containing fluids in a patient with
impaired regulatory mechanism.
 Diminished function of the homeostatic mechanism responsible for regulating
fluid balance.

26. CONT
 Sodium retention and build up of too much fluid in the intravascular space.
 Fluid volume excess or hypervolemia or over hydration.

27. CLINICAL MANIFESTATION
o Edema
o Unexplained and rapid weight gain
o Swelling in arms and legs
o Distended neck veins
o Crackles
o Tachycardia
o Shortness of breath(dyspnea)
o Increased blood pressure
o Increased pulse pressure
o Increased central venous pressure
o Increased weight
o Increased urine out put
o Shortness of breath and wheezing
o Fluid in abdominal cavity(ascites)
o Pulmonary edema
o Headache
o Confusion
o Lethargy

28. DIAGNOSTIC EVALUATIONS
 Physical examination
 Medical history
 Abdominal Ultrasound
 Albumin level
 Chest x-rays
 Electrocardiogram (ECG or EKG)
 Glomerular filtration rate (GFR)
 Liver enzymes
 Urinalysis
 BUN level and hematocrit (tends to
decrease because of hemodilution)
 Urine sodium level are increased if
the kidneys are attempting to
excrete excess volume.
 Urine sodium can be decreased in
case of cirrhosis, heart failure,
nephrotic syndrome.
 Specific gravity of urine dimishes.

29. MEDICAL MANAGEMENT
 Diuretics:
Furosemide (Lasix) is a loop diuretic that causes kidneys to excrete
sodium and water.
 Thiazide diuretics:
Thiazide diuretics (hydrochlorothiazide), (trichloromethi- -
-azide), (methychothiazide), block sodium reabsorption in distal tubules.
 Discontinuation of sodium containing fluids if administered.
 Restricting fluids and sodium
 Hemodialysis:
If kidneys are severely impaired.

30. HYPONATREMIA
 Decreased serum sodium levels (<135mEq/L.
 Sodium and chloride has the highest extracellular concentration,
 Deficits in kidneys functions are often the cause: drugs, disease, age, etc.
 Sodium deficits cause plasma/fluid hypo-osmolality and cellular swelling,
 Osmolality is defined as “the concentration of particles dissolved in a fluid.”
 The osmolality of serum can help diagnose several medical conditions such as
dehydration, diabetes, and shock.
CAUSES:
Pure sodium loss
Low intake
Dilutional hyponatremia

31. CLINICAL MANIFESTATION
 Remember, sodium is involved
with action potentials in neurons
and muscles, overall cell volume
(osmotic) as well as other cell
functions.
 Most life-threatening cerebral
edema, and increased intracranial
pressure.
 Lethargy , confusion, decreased
reflexes, seizures, and coma.
 If leads to loss of ECF and
hypovolemia, hypotension,
tachycardia, decreased urine out
put.
 If dilutional from excess water
(hypervolemic hyponatremia), see
weight gain, edema, Ascites, jugular
vein distention

32. DIAGNOSTIC EVALUTION
 Physical examination.
 Medical history
 Serum sodium level
 Decreased serum osmolality
 Increased urinary sodium secretion
 Urine R/E
 Decreased Urine specific gravity
 Fluid status

33. TREATEMENT
 I/V Fluids : normal saline, etc.
 Fluid restriction.
 Steroid's
 Angiotensin converting Inhibitors
 Chemotherapy
 Adjusting diuretics
 Vaptans (e.g. Tolvaptan) block ADH secretion

34. HYPERNATREMIA
 Increased serum sodium level from normal level >135-145 mEq/L
 High sodium causes an increase in ECF tonicity which draws water out of the
cell resulting in cellular dehydration
 Generally caused by decreased water intake or increased water loss
 More common in infants and those who can’t express thirst (elderly)
 Hypodipsia : Inability to express thirst.

35. CLINICAL MANIFESTATIONS
o Dry skin
o Decreased tissue turgor
o Decreased salivation
o Elevated body temperature
o Hypovolemic hypernatremia
 Thirst
 Confusion, seizures, coma.
 Nausea, vomiting, excessive
sweating.
 Weight loss, generalized weakness
 Pitting edema
 Agitation
 Hyper reflexia
 Subcortical and subarachnoid
hemorrhage

36. DIAGNOSTIC EVALUATIONS
 Serum sodium >145 mEq/L.
 Urine sodium <40 mEq/L.
 High serum osmolality
 Increased urine specific gravity
 Urine R/E

37. TREATEMENT
 Replacing water: orally or I/V Normal saline , 5% DW.
 Diuretics: Thiazide or loop diuretics.
 Sodium restriction: low sodium diet 500 – 2000 mg/day
 Treating underlying diseases.

38. HYPERKALEMIA
 Normal level is 3.5 to 5.0 mEq/L.
 Maintains intracellular osmolarity (high concentration in cells).
 Increased ECF potassium levels >5.0 mEq/L.
 Caused by excessive intake or decreased excretion in urine in the kidneys.
 MANIFESTATIONS:
Initially causes hyper excitability, but at a very high level of
potassium the membrane potential approaches to threshold and may prevent
repolarization and subsequently depolarization.
 Weakness, fatigue, muscle cramps, decrease cardiac response
 Hyperkalemia is a rare disorder because of efficient renal excretion.

39. DIAGNOSTIC EVALUATION
 Elevated Serum level.
 Blood tests
 Urinalysis
 ECG
TREATEMENT:
Treatment should be started with calcium gluconate to
stabilize cardiomyocyte membranes, followed by insulin injection, and b-
agonists administration. Hemodialysis remains the most reliable method to
remove potassium from the body and should be used in cases refractory to
medical treatment.

40. HYPOKALEMIA
 Potassium level <3.5 mEq/L.
 Potassium balance is described by changes in plasma potassium levels