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Chapter Seven: The Total Body Water and The Plasma Sodium Concentration
Podcast summary created with Snipd AI
Quick takeaways
- Understanding total body water compartments aids in medical calculations and treatment planning.
- Sodium distribution impacts osmolality regulation and fluid volume control in clinical settings.
- Calculating plasma osmolality with sodium and potassium levels is essential for managing electrolyte imbalances effectively.
Deep dives
Understanding Total Body Water Distribution
Total body water distribution involves three major compartments: intracellular, interstitial, and vascular spaces. The book discusses the distribution percentages for each space, where two-thirds is for intracellular, one-third for extracellular, and further division among interstitium and plasma. These ratios may vary slightly in practice and are crucial in medical calculations.
Significance of Sodium Regulation
Sodium plays a vital role in determining osmolality and body fluid volume regulation. Studies on astronauts and critically ill patients reveal the dynamic nature of sodium distribution within the body. The exchangeable sodium and potassium amounts, in addition to total body water, are integral in understanding plasma sodium levels and their implications in different medical contexts.
Calculating Effective Plasma Osmolality
The podcast delves into calculating effective plasma osmolality through formulas involving sodium, potassium, and total body water. By determining the exchangeable sodium and potassium and their contribution to plasma osmolality, clinicians can better comprehend osmotic balance and its impact on physiological processes.
Clinical Application of Osmolality Concepts
The exchangeable sodium and potassium concepts find practical application in clinical scenarios like treating hyponatremic, hypokalemic patients. Understanding how sodium and potassium shifts influence plasma sodium levels is crucial in managing electrolyte imbalances effectively. This knowledge can aid in mitigating risks of conditions like central pontine myelinolysis, especially in complex medical cases.
Understanding Central Pontine Myelinolysis
Central pontine myelinolysis challenges the traditional understanding of cellular dehydration, as giving potassium to a dehydrated cell should lower sodium levels. However, observations show cases where patients overcorrect their sodium levels unpredictably. This perplexing condition emphasizes the complexity of cellular dehydration mechanisms and the risks of rapid electrolyte shifts.
Exploring Starling's Law and Interstitial Fluid Dynamics
Starling's Law governs fluid movement across capillary walls, with hydrostatic and oncotic pressures balancing fluid filtration. Movement between plasma and interstitial compartments occurs mainly at post-capillary venules, impacting fluid exchange. Understanding these capillary dynamics highlights the role of osmolarity, plasma protein permeability, and interstitial pressures in maintaining fluid balance and preventing edema.
Chapter 7
References
Sands JM, Blount MA and Klein JD. Regulation of Renal Urea Transport by Vasopressin. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116377/
In this invited piece, Sands and colleagues explain that although urea is permeable across membranes, this is slow, thus urea transporters in the kidney, under control of vasopressin, are needed to facilitate transport and create the medullary gradient.
Text book using 20% of extracellular compartment being in the intravascular compartment. https://courses.lumenlearning.com/ap2/chapter/body-fluids-and-fluid-compartments-no-content/
The chapter I wrote where I went through the math in figure 7-3. It was a major revelation to me: https://docs.google.com/document/d/17BM1xihvlztuQlU8GVNhEDoPLzr6GounHYZAtVUkLvw/edit?usp=sharing
Association Between ICU-Acquired Hypernatremia and In-Hospital Mortality https://journals.lww.com/ccejournal/fulltext/2020/12000/association_between_icu_acquired_hypernatremia_and.26.aspx
Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients https://pubmed.ncbi.nlm.nih.gov/30948456/
Edelman IS, Leibman J, O’Meara MP and Birkenfeld LW. Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. JCI 1958. This classic paper calculates the total body exchangeable sodium and potassium and establishes the relationship between these. Understanding this painstacking work helps understand the effect of supplementing potassium in the setting of hyponatremia.
https://dm5migu4zj3pb.cloudfront.net/manuscripts/103000/103712/cache/103712.1-20201218131357-covered-e0fd13ba177f913fd3156f593ead4cfd.pdf
Edelman is the Root of Almost All Good in Nephrology https://www.renalfellow.org/2014/11/20/edelman-is-root-of-almost-all-good-in/
Jens Titze and his team published a pair of articles that shocked those interested in salt and water in JCI in 2017.
High Salt intake reprioritizes osmolyte and energy metabolism for body fluid conservation https://www.jci.org/articles/view/88532
Increased salt consumption induces body water conservation and decreases fluid intake https://www.jci.org/articles/view/88530
in this exciting exploration of the basic assumptions that we hold true regarding salt and water (and staring Russian cosmonauts and an incredible controlled simulation of salt and water intake), Titze shows that high sodium intake does not simply drive water consumption (as we usually teach) but instead leads to a complex hormonal and metabolic response (even with diurnal variation!) and results in body water conservation and decreased water consumption.
And accompanying editorial from Mark Zeidel: salt and water, not so simple. https://www.jci.org/articles/view/94004
In addition, Titze and others have done interesting work on sodium deposition in tissues where it may also be a source for systemic inflammation.https://pubmed.ncbi.nlm.nih.gov/28154199/
Jens Titze talking about salt, water, thirsting a TEDx talk. https://www.youtube.com/watch?v=jQQPBmnIuCY
A discussion/debate of the overfill vs. underfill theory of edema in the nephrotic syndrome (hint- overfill theory triumphs) would be incomplete without a reference to congenital analbuminemia. This reference from Frontiers in Genetics explores the diagnosis, phenotype and molecular genetics and reveal that patients tend to have only mild edema but severe hyperlipidemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478806/
The finding that proteinuria can directly lead to sodium retention based on a study when puromycin aminoglycoside induced proteinuria of one kidney lead to sodium retention by that kidney which was localized to the distal nephron. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436841/?page=9
Plasmin may be the culprit at the level of the epithelial sodium channel based on Tom Kleyman’s work: https://jasn.asnjournals.org/content/20/2/233
Amiloride may help! (stay tuned for amiloride in a future episode) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6016639/
An old favorite of JC’s from the Kidney International feature which debates the cause of edema in the nephrotic syndrome.
https://www.sciencedirect.com/science/article/pii/S0085253815583075
Under protest, we hobbled through a discussion of the Gibbs Donnan affect even encouraged by one of Amy’s fellows based on this article from QJM: https://academic.oup.com/qjmed/article/101/10/827/1520972 suggesting that our understanding of the role of hyponatremia in fractures might be all wrong- it could be related to hypoalbuminemia.
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