Hypervolemia, definition, etiology, clinical feature, diagnosis, and how to manage it.

1. Topic 2. Hypervolemia:

2. • Is an overload of body fluid that results when
there is an excessive intake or decreased
excretion of fluids.
• When the total volume of fluid in the body is
increased, the workload on the heart and the
pressure on the blood vessels are increased.
• Fluid accumulation may result in expansion of
interstitial volume, blood volume or both.
•

3. Sign and symptoms

4. • Physical
appearance:
1. Weight gain.
• Cardiovascular:
1. Raised jugular venous
pressure.
2. Added heart sounds.
3. Basal crackles.
4. A raised arterial blood
pressure.
• Respiratory:
1. Dyspnea
2. Pulmonary oedema.
3. Pleural effusions.

5. • Gastrointestinal:
1. Ascites.
• Skin:
1. Edema in ankle, face
“morning”, and sacral
“bed”.
2. Poor wound healing.
3. Pressure sores.
• Central Nervous
System:
1. Headache.
2. Loss of cognitive
abilities.
3. Confusion.
4. Delirium.
5. Seizures.
6. Coma.
• Systemic edema:
1. Anasarca.

6. Ankle edema

7. Facial edema

8. Sacral edema

9. Pressure sore

10. anasrca

11. Etiology of Hypervolemia:
• HEART FAILURE.
• HEPATIC CIRRHOSIS.
• NEPHROTIC SYNDROME.
• Drug causes renal sodium retentions:
a) Oestrogens.
b) Mineralocorticoids and liquorice.
c) Non-steroidal anti-inflammatory drugs (NSAIDs).
d) Thiazolidinediones.
• Complement-deficiency syndrome; with therapeutic
use of interleukin 2.

15. • Idiopathic edema:
a) Women without heart failure, hypoalbuminaemia,
and renal or endocrine disease.
b) Diuretic-dependent sodium retention.
• Local increase in edema :
a) Ankle oedema = due to venous or lymphatic
damage following thrombosis or surgery.
b) Ankle or leg oedema due to immobility.
c) Oedema of the arm due to subclavian thrombosis.
d) Facial oedema due to superior vena caval
obstruction.

16. • HORMONAL CHANGES:
1. Premenstrual syndrome
2. Pregnancy
• MEDICATION:
• Birth control pills, hormone replacement therapy,
antidepressant, certain antihypertensive drugs
• INTRAVENOUS SUBSTANCES:
A. IV solutions.
B. Blood transfusion.
C. IV medications “hypertonic fluid [mannitol,
hypertonic saline solution] + albumin”.
D. Diagnostic contrast dyes.

17. Investigations

18. • HISTORY AND PHYSICAL EXAMINATION:
• As mentioned in sign and symptoms.
• LABORATORY:
o Sodium test from serum and urine.
o Kidney function test.
o Liver function test.
• MEDICAL IMAGING:
Chest x- ray = cardiomegaly and effusion of
pericardium and pleural, pulmonary edema.
Ultrasound = ascites and liver shrinkage.
ECG and Echocardiography.

19. Pulmonary edema
Pleural effusion
Cardiomegaly
Ascites with liver cirrhosis

20. Management

21. • Limitation intake of:
1. Water and fluid.
2. Salt.
3. Drugs.
• Medication:
• Diuretics:
a) Thiazide diuretics:
b) Potassium-sparing diuretics:
c) Carbonic anhydrase inhibitors.
d) Aquaretics (vasopressin or ADH antagonists)
e) Sodium–glucose co-transporter 2 (SGLT2)
inhibitors [e.g: canagliflozin].

24. Mechanism action of carbonic
anhydrase:

25. Mechanism action of mannitol:

26. Mechanism action of frosemide

27. Mechanism action of Thiazide:

28. Mechanism action of Potassium
sparing:

29. Mechanism action of ADH Antagonist:

30. Mechanism action of SGLT 2 inhibitors

31. 1. Poor bioavailability.
2. Reduced GFR, which may be due to
decreased circulating volume despite
oedema (e.g. nephrotic syndrome, cirrhosis
with ascites) or intrinsic renal disease.
3. Activation of sodium-retaining mechanisms,
particularly aldosterone.
Resistance to diuretics

32. • How t over come for this resistance?
• Intravenous administration of loop diuretic “e.g
furosamide = a maximum of 2 g for an adult
because of ototoxicity”.
• Intravenous administration of albumin solutions
restore plasma oncotic pressure temporarily in
the nephrotic syndrome but do not increase the
natriuretic effect of loop diuretics.
• Combinations of various classes of diuretics
“e.g A loop diuretic plus a thiazide”