Page created on December 18, 2018. Last updated on December 18, 2024 at 16:56
Causes:
| Hypotonic hypervolaemia (more water is gained than salt) | Normotonic hypervolaemia (salt and water gain are equal) | Hypertonic hypervolaemia (more salt is gained than water) |
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Hypotonic hypervolaemia:
Enhanced water intake can occur in psychiatric patients or people trying to win stupid contests.
In severe renal failure is there severe hyposthenuria/asthenuria, so the kidneys can’t adapt to an increased water intake.
SIADH stands for syndrome of inappropriate antidiuretic hormone and is a condition where the levels of ADH is abnormally high. It can occur in paraneoplastic syndrome, in problems with the brain and in situations of severe stress, because ADH is also a stress hormone. It’s especially common during surgery. When ADH is very high will a lot of water initially be retained. However, the kidneys will eventually increase urine output to compensate, thereby causing hypotonic normovolaemia.
In severe oedema will RAAS be activated because of low plasma volume, but the extra retained water and salt will just travel into the interstitium to make the oedema larger instead of normalizing the plasma volume. In severe oedema can the hypovolaemia be so severe that ADH is secreted, causing hypotonicity.
Glucose infusions are isotonic by themselves, however they’re often given to patients that need the glucose, such as in patients that have recently been operated on. As soon as this infusion is given will the cells absorb the glucose, making only water remain in the ECS.
Normotonic hypervolaemia:
IV saline is isotonic.
In healthy people will and increased salt intake cause increased water retention, meaning that a normotonic hypervolaemia develops.
In mild and moderate oedema will RAAS be activated but not AVP, meaning that the hypervolaemia remains normotonic.
Hypertonic hypervolaemia:
Conn syndrome is a primary hyperaldosteronism, leading to increased salt and water retention.
Cushing syndrome is a primary hypercortisolism. Cortisol also acts on mineralocorticoid receptors. The exact mechanism of how this elevated mineralocorticoid activity causes hypertonic hypervolaemia and not normotonic hypervolaemia is something I don’t understand.
Extreme salt intake is well tolerated in healthy adults, but not in young children and people with oligura.
Consequence of hypervolaemia
- Haemodilution (low haematocrit)
- Oedema
- Hypertension
Whether the extra volume will stay in the intravascular space to cause hypertension, or move to the interstitial space to cause oedema, depends. It depends entirely on the Starling forces in the capillaries, i.e. how much fluid is going in and out. That depends on the hydrostatic pressure and the oncotic pressure.
In heart failure or portal hypertension will there be venous congestion which causes increased hydrostatic pressure in the capillaries. If hypervolaemia occurs then will the extra fluid be extravasated into the interstitial space, causing more oedema.
Oedema also occurs when the oncotic pressure decreases due to fewer proteins in the plasma, often due to protein malnutrition, nephrotic syndrome or liver disease.
Lastly can extravasation occur during inflammation. This is not as important when talking about hypervolaemia though.
Compensation of hypervolaemia
If the fluid stays in the intravascular space will BP increase. This decreased the RAAS activation, causing more salt and water excretion.
If the fluid moves to the interstitial space will the plasma volume actually decrease. RAAS only detects the changes in plasma volume and not in the interstitial volume, so RAAS will increase, causing K+ loss but salt and water retention, potentially making the oedema even worse.
Natriuretic factors like atrial natriuretic peptide and brain natriuretic peptide will increase, which increases sodium excretion and thereby water excretion.