SODIUM & WATER BALANCE Flashcards
What are the three main regulators of sodium and water balance?
- Antidiuretic hormone
- Sympathetic nervous system
- RAAS
What is the major determinant of effective circulating volume?
Which three main factors modify ECV?
SODIUM
- High sodium → increased ECV
- Low sodium → decreased ECV
- Volume
- Cardiac output
- Vascular resistance
How can you clinically gauge the effective circulating volume?
Measure blood pressure, particularly lying/standing
Why does bodyweight go up after a salty meal?
Body will release ADH to retain water and maintain sodium balance
What will increased sodium consumption do to the sympathetic nervous system and RAAS? If salt consumption is chronically high, what will happen to the ECV, explain why this occurs.
Sodium increases ECV due to ADH. This decreases SNS + RAAS, decreasing sodium retention ⇒ restoration of sodium balance.
SNS + RAAS maintain SODIUM not ECV. Thus, ECV remains high and SNS / RAAS will not decrease ECV back to baseline. Baseline will only be reached once salt intake is reduced.
What are the two main clinical signs of high ECV caused by sodium?
…low ECV caused by sodium?
- Weight gain/loss respectively
- Hypertension/improvement in hypertension respectively
Why is it easy to develop hyper or hyponatraemia in the context volume losses such as nausea, vomiting and diarrhoea?
- ADH released in high osmolality unless severe volume loss, in which case release driven by volume receptors
- ADH remains high as no longer controlled by sodium
- Water retained by kidneys, sodium determined by intake/losses rather than osmolality
Why do people with GI losses often develop a hyponatraemia rather than hyper?
Usually drink free water as easier on stomach and don’t eat → hyponatraemia
(Hypernatraemia can occur if they are not taking enough free water)
By what mechanisms does heart failure cause chronically elevated sodium?
why is ADH chronically elevated in this case?
- Decreased ECV due to low CO → chronic activation of SNS + RAAS
- Sodium chronically retained
- ADH chronically activated DUE TO LOW ECV: Free water chronically retained to maintain sodium balance
Important note: ADH activation in heart failure is NON-OSMOTIC (due to low ECV)
In someone with a healthy heart increased consumption of salt will increase ECV. In heart failure ECV does not increase normally with fluid retention due to failing heart being unable to increase CO. This results in congestion, what are the three clinical signs of congestion?
- Pulmonary oedema
- Elevated JVP (internal jug; classic sign of venous HTN (e.g. R heart failure)
- Pitting oedema
How do you assess total body sodium level?
Assessing if the patient is clinically hyper, hypo or euvolemic
Why is the volume status of a patient normal in SIADH?
What will the three clinical findings be? Explain each one
- Water retention → increased effective circulatory volume → decreased SNS/RAAS → sodium excretion → decreased effective circulating volume (back to normal)
Key findings:
- hyponatraemia (water retention)
- normal volume status (SNS + RAAS dialled down)
- concentrated urine (ADH high)