This presentation help u to understand the loss of water and electrolyte in the human body

1. Topic 3. Hypovolemia:

2. • Is a deficiency of body fluid that results when
there is a total decrease in the fluid volume in
the body.
• Types:
• Fluid volume deficit— the loss of water and
sodium from the body.
• Dehydration— the loss of water from the
body in excess of sodium, resulting in an
increased osmolality.

3. Consequence of hypovolemia
• Decreased blood volume leads decreased
oxygen and nutrients to the tissues.
• Loss of cellular and tissue function that leads
organ failure and death.
• Changed osmolality may lead cell shrinkage
or swelling.

4. Hypovolemia stimulates:
1) The release of renin and then angiotensin II
and eventually aldosterone.
2) Vasoconstriction to attempt to maintain blood
pressure and circulation (renin).
3) The reabsorption of sodium and water
(aldosterone) to restore volume.
4) The thirst center in an attempt to restore
volume through increased intake.

5. Hypovolemia Has 3 Form “Relative To
Sodium Loss”:
Type Water (H2O) Sodium (Na)
Isotonic
hypovolemia.
(+) lost (+) lost
Hyponatremic
hypovolemia
(+) lost may be
partially replaced
(++) lost
Hypernatremic
hypovolemia
(++) lost (+) lost may be
partially replaced.

6. Sign and symptoms

7. • Cardiovascular:
1. Hypotension
(Orthostatic
hypotension).
2. Tachycardia.
3. Tachypnea.
4. Weak pulse.
• Skin:
1. Dry.
2. Decreased skin turgid.
3. Blanching of skin.
• Gastrointestinal:
1. Dry mucous
membranes.
2. Nausea.
3. Vomiting.
4. Decreased bowel
sounds.
5. Diarrhea.

8. Hypotension
Tachcardia
Weak pulse
blenching

9. Nausea Vomiting
Cold extremities
irritability
Decreased urine
output
Diarrhea

10. • Extremities:
1. Cold.
2. Decreased capillary refill (>
5 seconds).
3. Muscle cramps.
• Central nervous
system:
1. Irritability.
2. Thirst.
3. Confusion.
4. Coma.
5. Decreased sensorium.
• Renal:
1. Decreased urine output.
2. Concentrated urine.

11. Etiology of Hypovolemia:
1= Renal:
• Diuretic use.
• Impaired tubular sodium conservation.
• Reflux nephropathy.
• Papillary necrosis (Analgesic nephropathy, Diabetes
mellitus and Sickle cell disease).
• Bartter's syndrome “ failure of sodium chloride
absorption by the thick ascending limb of the nephron
characterized by:
• Excessive production of prostaglandins, + sodium chloride
wasting + juxtaglomerular hyperplasia + high renin levels,
and secondary hyperaldosteronism }”

12. Papillary necrosis
Reflux nephropathy

13. 2= Extra renal:
Septicemia.
Hamorrhage (External, Concealed, e.g. leaking
aortic aneurysm).
Burns.
Other system:
o Gastrointestinal losses:
1. Vomiting and Diarrhoea,
2. Pancreatitis.
3. Intestinal obstruction.
4. Ileus.
5. Nutritional hypoalbuminemia.
6. Peritonitis.

14. Sepsis
Burns Hemorrhage

15. o Skin respiratory system:
1. Fever “Perspiration”.
2. Heat exposure.
3. Profuse sweating.
o Respiratory:
1. Hyperventilation.
o Endocrine :
1. Aldosterone deficit (Addison’s disease).
2. Deficiency of anti diuretic hormone (diabetic
insipidus).
3. Diabetic mellitus.

16. Fever
Heat exposure
Profuse sweating
Hyperventilation

17. Investigations

18. • CLINICAL:
o 3 reliable signs:
Decreased Jugular venous pressure.
Orthostatic tachycardia (an increase of >15–20
beats/min upon standing).
Orthostatic hypotension (a >10–20 mmHg drop
in blood pressure on standing).
o Central venous pressure: both basal and after
intravenous fluid challenge.
o Peripheral cyanosis.

19. o Cold extremities.
o Urine output measurements at regular
intervals = Oliguria.
o Altered mental status.
o Chest X-ray.
o Serial weights of the patient.

20. • LABORATORY:
Elevated hematocrit.
High specific gravity.
Increased plasma osmolarity.
Increase in blood urea nitrogen (BUN) and
creatinine.
Increase in plasma K+ concentration.
Increaesd liver function tests and cardiac
biomarkers.
Acid-base disorders “lactic acidosis and increased
anion gap”.
Urine Cl– concentration <25 mM.
Urine osmolality is high.

21. Management

22. Medication through Oral:
• In case of vomiting, diarrhoea or excessive renal
losses:
• Oral water and sodium salts.
• In case of renal salt wasting:
• Sodium chloride (600 mg, approximately 10 mmol
each of Na+ and Cl- per tablet), the usual dose of
which is 6–12 tablets/day with 2–3 L of water.
• In case of Chronic Kidney Disease, postobstructive
renal failure, renal tubular acidosis:
• Sodium bicarbonate (500 mg, 6 mmol each of Na+
and HCO3- per tablet) is given in doses of 6–12
tablets/day with 2–3L of water.

23. Medication through Intravenous line:
• In case of hemorrhage:
• Mild hemorrhage = infusing normal saline.
• Acute or sever haemorrhage = infusion of a
combination of red cells and a plasma substitute or
whole blood.
• In case of burns or severe peritonitis:
• Infusion of human plasma or a plasma substitute.
• In critically ill patients or persistent renal
dysfunction:
• Infusion of crystalloids (Hartmann’s solution or
Plasma-Lyte, which have lower chloride
concentrations than saline).

24. • In case of hypotension and evidence of impaired
organ perfusion (e.g. oliguria, confusion):
• Rapid infusion (e.g. 1000 mL per hour or even faster)
of 0.9% NaCl. “PULMONARY OEDEMA”
• Slow infusion of 1000 mL every 4–6 h.
• In case of surgery:
• Infusion of normal saline 1–2 L can be given over 24
h.
• In case of diabetes insipidus, excessive sweating or
unable to drink (e.g. after surgery):
• 5% glucose with K+ because pure water would lead
to osmotic lysis of blood cells.

25. • In case of nutritional hypoalbunemia, or burns:
• In fusion of colloid-containing solutions (iso-
oncotic albumin solutions and plasma) less half
life and cost.
• In case of sepsis and inflammatory process:
• Intravenous antibiotic + Iv fluid.
The nurse must monitor the patient closely during
and after fluid replacement therapy because as
fluid returns to the blood vessels from the tissues
or as blood vessels constrict to normal diameter,
fluid volume overload can result.
Hypervolemia……

26. How to monitor:
• Fluid balance charts.
• Body weight.
• Plasma biochemistry ‘is crucial’.