quick questions about Na level in Low Volume states!

[hunteradam07]

i was wondering what is the serum Na in Low vol states? Since aldosterone would kick in and increase reabsorption at DCT, it would increase. However, Dr. ******* (pass program) said that hyponat states accompanied with low vol states and he explained as dilutional effect. Can someone confirm this? And if this is the case would patients like to be in high depolarize states interm of cellular level? Since hyponatriema would cause more like to depolarize states according to Dr. ******* as well due to Ca and Mg rush into cell. Thanks for u time.

[Dr. X]

i was wondering what is the serum Na in Low vol states? Since aldosterone would kick in and increase reabsorption at DCT, it would increase. However, Dr. ******* (pass program) said that hyponat states accompanied with low vol states and he explained as dilutional effect. Can someone confirm this? And if this is the case would patients like to be in high depolarize states interm of cellular level? Since hyponatriema would cause more like to depolarize states according to Dr. ******* as well due to Ca and Mg rush into cell. Thanks for u time.

It depends on the reason why there is a low volume state [in ecf]. Its possible to have low volume state.. say diarrhea but you lose isotonic loss.. so serum na is not affected. In another low volume state, say in adrenocortical deficiency.. (lack of aldosterone), you would lose out more na+ than water.. so you become hyponatremic.

To get into dilutional effect: lets say you have less sodium in your ecf. the osmalarity of ECF decreases.. (less sodium more water). To equilibrate to this change in the ICF, ie. it has to decrease its osmalarity too to equal it with ecf. It sucks up the water from ecf into icf. Thus, you get swelling of the icf, and loss of water in ecf.

as for depolarization.. maybe lil more input would help or change of phrase.

[hunteradam07]

I know about the fluid shift, but not what i mean though. I jz want to know about how hyperna or hypona or electrolytes inbalance effect cellular depolarization ie what channel and how? Thanks for u input though.

[Dr. X]

• Hyperkalemia: Tall “tented” T waves, absence of P waves, wide QRS complex
• Hypokalemia: Flat/small T waves, U waves are also seen
• Hypercalcemia: short QT interval
• Hypocalcemia: prolonged QT
• Digoxin: ST depression and T wave inversion

these are some electrolyte imbalances that are hy. you could translate the ecg reading to figure out the depolarization and repolarizations abnormalities.

I really havent come across any significant source which divulges into na+ imbalance affecting the depolarization or repolarization. They focus on swelling of the cell or not, both ways causing a CNS disturbance. Remember how goljan asked us to picture the whole brain being one cell that is either affected by hypo- or hypernatremia.. both capable of causing altered mental status. "Na+ channel" responsible for transporting na+ and k+ could be misinterpreted because defects in the channel itself or dysregulation of the ions itself could affect the depolarization. However, potassium is often involved.

here are some thoughts that ran in my head in terms of na+.. jus a thought. In ligand gated channels.. na+ doesnt play much of role since neurotransmitters are what controls the influx of na. Also, in voltage gated channels, the inward sodium is limited by threshold. maybe its jus irrevelant.

nehoo, when it comes to hypo or hyper natremia.. its def. HY to think of "cerebral edema" and "fluid shifts", thus focusing on neurologic symptoms and signs of hyrdation/dehydration.

[hunteradam07]

I know what u mean interm of fluid shift and celebral edema. However, the dr. from Pass Program really makes a big deal about different electrolytes imbalance causing different depolarize or repolarize states and it links to clinical. I jz want to know if it's correct. So if anyone could tell me about that concepts, i would appeciate a lot. Thanks folks.

[Citdawg98]

Originally Posted by hunteradam07

I know what u mean interm of fluid shift and celebral edema. However, the dr. from Pass Program really makes a big deal about different electrolytes imbalance causing different depolarize or repolarize states and it links to clinical. I jz want to know if it's correct. So if anyone could tell me about that concepts, i would appeciate a lot. Thanks folks.

I hope this might help... The Low Volume State....

Long term Control of BP

• Stimulate JG apparatus- by low flow to the kidneys.
  • Renin comes out
  • Cuts Angiotensinogen (formed in liver) to Angiotensin I
  • Angiotensin I is converted by ACE (in lungs) to Angiotensin II
  • Angiotensin II
    • Very potent vasoconstrictor
    • ­ TPR
    • ­BP
  • Ag II will also stimulates Aldosterone
    • To decrease loss of volume
    • Aldosterone goes to kidney and reabsorbs Na from DCT
    • Excretes K in the process.
      • Serum Na will be diluted and decreased. Because Na brings in 3x the Water!!!
      • Serum Cl will also decrease due to dilution
      • Serum K will decrease because of secretion
      • Also excretes H+
        • Serum pH will go up

LOW VOLUME STATE (after chronic period of time)
Will present with:

• Hypertension
• ­TPR → Renin/Angio System
• ¯Na → Aldosterone
• ¯K → Aldosterone
• ­pH (metabolic alkalosis)
  • Examples:
    • CHF
    • Pregnant woman with emesis
    • Child with projectile vomiting
    • Patient with renal artery stenosis
    • Exercise
    • ANY TIME ↓ Blood flow to the kidneys!!!

3 Exceptions: Low volume states that present with METABOLIC ACIDOSIS
1. Diarrhea → loss of HCO3-
2. DKA → ↑ ketones
3. RTA II – loss of HCO3-


Now, from what I have read...and remember..The different depolarization states for Na, K, Cl, Mg, Ca all play a large role in the more or less wanting to depolarize...too much K causes overshoot (I think) and if there is not enough Na the cell can't reset to go again... I hope this helps...

[Water]

In extreme case of fluid loss, adrenal gland does not respond to agiontensin II. So aldosterone won't be released. ADH will be released in response to low blood volume. This increases water permeability in the collecting duct and distal part of the distal convoluted tubule. Increasing water reabsorption with not so much of sodium causing the dilutional effect.
In hyponatremia, extracellular is less positive so K leaves intracellular space. This makes intracellular compartment to become more negative and hyperpolarized. Please correct if I make any mistakes.

[shygal122]

In kaplan physio the Dr explains that ECC of sodium does not affect depolarization the way high or low levels of potassium would.