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Sodium and Water Homeostasis

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Sodium and Water Homeostasis, Fluid Homeostasis, Sodium Hemeostasis, Fluid Shifts, Osmoregulation, Water-Electrolyte Balance, Sodium, Sodium Cation, Fluid and Electrolyte Balance

  • Physiology
  • Total blody water distribution
  1. See Total Body Water
  2. Total Body Water (TBW) accounts for 60% of body weight in men (50% in women)
    1. Example: 70 kg man has ~42 L TBW and a 70 kg woman has ~35 L TBW
  3. Intracellular fluid volume or ICFV (66% of Total Body Water)
    1. Example: 70 kg man has ~28 L ICFV and a 70 kg woman has ~23 L ICFV
    2. High concentrations of Potassium (>130 mEq/L) and Magnesium (>20 mEq/L)
    3. Low concentrations of Sodium (<20 mEq/L)
  4. Extracellular fluid volume or ECFV (33% of Total Body Water)
    1. Example: 70 kg man has ~14 L ECFV and a 70 kg woman has ~12 L ECFV
    2. Electrolytes
      1. Low concentrations of Potassium (<5 mEq/L) and Magnesium (<2 mEq/L)
      2. High concentrations of Sodium (135-145 mEq/L)
    3. Interstitial volume (75% of extracellular fluid)
    4. Plasma volume (25% of extracellular fluid)
      1. Plasma volume is maintained by plasma proteins via oncotic pressure
  5. Images
    1. TotalBodyWater.png
  • Physiology
  • Sodium and water
  1. Total Body Water is primarily maintained via extracellular Sodium concentration
    1. Extracellular Sodium is maintained at 135-145 mEq/L
    2. Sodium (Na+) is the primary osmole to maintain extracellular fluid volume
  2. Total body Sodium is typically estimated based only on extracellular Sodium
    1. Intracellular Sodium is negligible (<20 mEq/L) compared with extracellular Sodium (>135 mEq/L)
  3. Water follows higher Sodium concentrations (osmotic pressure gradient)
    1. Increased Sodium concentrations results in greater extracellular water retention
      1. Results in Fluid Overload (Edematous State) with increased ECFV
    2. Decreased Sodium concentration results in extracellular water loss
      1. Results in volume depletion with decreased ECFV
  4. Sodium is regulated to maintain appropriate extracellular fluid volume
    1. Sodium homeostasis balances Sodium intake with Sodium excretion
    2. Fluid Overload and Hypovolemia are defects in Sodium regulation (even when Serum Sodium is normal)
    3. Hyponatremia is a water excess state (water regulation abnormality)
      1. May be associated with low, normal or high ECFV (or total body Sodium)
  • Physiology
  • Osmolality and Tonicity
  1. See Serum Osmolality (and Extracellular Fluid Tonicity)
  2. Sodium is the chief osmole in maintaining plasma osmolality and tonicity
    1. Sodium is in greatest overall concentration of any solute in the extracellular fluid (osmolality)
    2. Sodium also has the greatest effect on ECF osmotic pressure gradient for attracting water
    3. Glucose, Sorbitol, and Mannitol also may generate, to a much lesser extent, an osmotic gradient
  3. Osmolal Gap
    1. Osmolality may be calculated based on known solutes (Sodium, Glucose, BUN)
    2. Osmolar Gap is the difference between expected and measured osmolality
    3. Osmolar Gap >10 mOsm/L suggests unmeasured solutes
      1. Example: Toxic Alcohols such as Polyethylene glycol
  4. Cellular hydration and tonicity
    1. Fluid Shifts into or out of cells are based on tonicity
    2. Rapid changes in extracellular Sodium concentration can seriously impact cell fluid (esp. brain cells)
      1. Rapid onset Hyponatremia, results in cell swelling
      2. Rapid onset Hypernatremia, results in cell shrinkage
  • Physiology
  • Sodium Regulation Mechanisms (Renally Mediated)
  1. Images
    1. renalSodiumWaterHomeostasis.png
  2. Nephron (Glomerulus and Renal Tubules)
    1. Sodium freely crosses the glomerular basement membrane
      1. Of filtered Sodium and water (180 L/day in a healthy 70 kg person), 65% is reabsorbed
      2. Sodium filtered through glomerulus into renal tubule has same initial concentration as blood
      3. Water follows Sodium through glomerulus
    2. Renal Sodium excretion is responsible for most Sodium loss
      1. Other causes of Sodium loss include sweating, Diarrhea, Hemorrhage and Burn Injury
    3. Glomerular Filtration Rate (GFR)
      1. Glomerular-Tubular Balance
        1. GFR is correlated with Sodium reabsorption in proximal tubule
        2. Decreased GFR results in decreased filtered Sodium and decreased Sodium and water reabsorption
        3. Increased GFR results in increased filtered Sodium and increased Sodium and water reabsorption
      2. Tubulo-Glomerular Feedback
        1. Glomerular Filtration Rate (GFR) is modulated by the Macula densa in the renal tubule
        2. Increased tubular flow at Macula densa results in afferent arteriole constriction and decreased GFR
        3. Decreased tubular flow at Macula densa results in afferent arteriole dilation and increased GFR
    4. Renal Tubules
      1. Water reabsorption (without Sodium) is in the descending loop of henle
      2. Sodium reabsorption (without water) is in the ascending loop of henle
        1. Results in hyperosmolar interstitium in the lower aspect of the loop of henle region
    5. Collecting Duct
      1. Collecting duct passes through the hyperosmolar interstitium and allows for further water reabsorption
      2. Collecting duct is porous, and water follows osmotic gradient into interstitium, concentrating the urine
      3. Antidiuretic Hormone (ADH) increases the collecting duct permeability to water (and water reabsorption)
  3. Renin-Angiotensin System (and Aldosterone)
    1. See Renin-Angiotensin System
    2. Afferent (sensory)
      1. Renal juxtaglomerular cells sense decreased renal perfusion and release renin
      2. Renin converts Angiotensinogen to Angiotensin I
      3. Angiotensin Converting Enzyme converts Angiotensin I to Angiotensin II
    3. Efferent (action)
      1. Angiotensin II stimulates aldosterone release from the adrenal cortex (zona glomerulosa)
        1. Aldosterone acts to increase Sodium absorption at the distal nephron (cortical collecting tubule)
      2. Angiotensin II increases proximal tubule Sodium absorption
        1. Sodium reabsorption is contingent on normal or acidic proximal tubule pH
          1. Sodium crosses from renal tubule cell into capillary with bicarbonate
          2. Bicarbonate crosses from renal tubule into renal tubule cell as CO2 via H+
          3. In alkalosis, H+ is lacking, bicarbonate (and Sodium) is less reabsorbed
  4. Atrial natriuretic factor
    1. See Brain Natriuretic Peptide (BNP)
    2. Afferent (sensory)
      1. Atria and vena cava respond to increased intravascular volume, filling and stretch
      2. Release atrial natriuretic factor from atria in response to increased volume
    3. Efferent (action)
      1. Overall effect is to increase Sodium (and water) excretion by blocking Sodium reabsorption
      2. Atrial natriuretic factor increases Glomerular Filtration Rate (GFR)
        1. Dilates afferent glomerular arteriole
        2. Constricts efferent glomerular arteriole
      3. Atrial natriuretic factor opposes Renin-Angiotensin System
        1. Decreases renal Sodium absorption at distal nephron (opposes Aldosterone)
        2. Inhibits renin secretion
  5. Sympathetic Nervous System
    1. Afferent (sensory)
      1. Aorta and carotid sinus receptors respond to decreased pressure (low volume)
      2. Activates Sympathetic System in response to volume depletion (decreased ECFV)
    2. Efferent (action)
      1. See Sympathetic Nervous System for effects
      2. Sympathetic System activation results in renal Sodium retention
      3. Mediated via Renin-Angiotensin System
  • Physiology
  • Water Regulation Mechanisms (affects osmolality and tonicity)
  1. Background
    1. Water intake and output mechanisms have greatest ECF Sodium concentration effect
  2. Thirst
    1. Potent Sensation that increases water intake and prevents Hypernatremia
      1. Hypernatremia is rare with intact thirst mechanism and adequate water access
    2. Inducers of thirst
      1. Increased extracellular fluid osmolality (responds to even a few mOsm/L difference)
      2. Angiotensin II
      3. Extracellular Fluid Volume depletion
  3. Antidiuretic Hormone (ADH or Arginine Vasopressin)
    1. Overall effect is to increase renal water reaborption
    2. ADH is released from the posterior pituitary
      1. Released in response to osmoreceptors in the hypothothalamus detecting hypertonicity
      2. Hypertonicity also stimulates thirst Sensation
    3. Response to increased plasma osmolality (and increased plasma Sodium concentration, Hypernatremia)
      1. Increased ADH secretion
      2. Water retention by the Kidneys
      3. Decreased plasma Sodium concentration (and decreased plasma osmolality)
    4. Response to decreased plasma osmolality (and decreased plasma Sodium concentration, Hyponatremia)
      1. Decreased ADH secretion
      2. Free water diuresis
      3. Increased plasma Sodium concentration (and increased plasma osmolality)
    5. Abnormal Antidiuretic Hormone
      1. Syndrome Inappropriate ADH Secretion (SIADH)
        1. Inappropriate ADH release, resulting in water retention despite normal Sodium and water status
        2. Results in Isovolemic Hypoosmolar Hyponatremia
      2. Diabetes Insipidus
        1. Excessive constant water diuresis due lack of pituitary ADH release or lack of renal response
  4. Renal mechanisms
    1. Renal responses
      1. Hypertonic response (e.g. Hypernatremia)
        1. Kidney retains water
        2. Urine is more concentrated than plasma
      2. Hypotonic response (e.g. Hyponatremia)
        1. Kidney excretes water
        2. Urine is more dilute than plasma
    2. Renal water regulation dependencies
      1. Adequate Glomerular Filtration Rate
        1. Concentrating and diluting mechanisms require a minimum GFR of 20% of normal
      2. Adequate renal tubule concentrating and diluting functions
        1. Adequate glomerular filtrate delivery to tubules
          1. Excessive proximal tubule water reabsorption bypasses the distal tubule
          2. Excessive proximal tubule water reabsorption may result in Hyponatremia
            1. Volume depletion (e.g. free water replacement of Diarrhea losses)
            2. Edematous States (e.g. CHF, Cirrhosis, Nephrosis)
        2. Adequate urine concentrating function (Ascending Loop of Henle)
          1. Ascending loop of henle reabsorbs 30% of Sodium into the Medullary interstitium
          2. Sodium (but not water) is reabsorbed via the Sodium-Potassium-2-chloride pump
            1. Sodium reabsorption in ascending loop of henle is blocked by loop diurectics
            2. However, Sodium may still be reabsorbed in distal convoluted tubule
              1. Therefore, Loop Diuretics cause less Hyponatremia and greater water loss
              2. Contrast with Thiazide Diuretics which block distal convoluted tubule
          3. Hypertonic Interstitium (via active Sodium reabsorption) allows for a concentrated urine
            1. Hypertonic Medullary interstitium attracts water from the collecting tubule
            2. Collecting tubule water permeability is increased by ADH (greater water reabsorption)
          4. Mediators decreasing interstitial hypertonicity and osmotic gradient (less water reabsorption)
            1. Decreased hypertonicity with Loop Diuretics
            2. Decreased hypertonicity with protein deficiency (nutritional deficiency)
              1. Urea (protein breakdown) also increases hyperosmolar interstitium
        3. Adequate urine diluting function (Distal Convoluted Tubule)
          1. Additional 5-10% of Sodium and chloride are reabsorbed at the distal convoluted tubule
          2. Sodium chloride reabsorption is blocked by Thiazide diurectics at the distal convoluted tubule
            1. Thiazide diurectics cause a relative retention of water more than Sodium
            2. Results in a greater risk of Hyponatremia than with Loop Diuretics
          3. Without later water reabsorption, the urine is dilute
      3. Adequate Antidiuretic Hormone (ADH) functioning
        1. ADH is key regulator of urine concentration and dilution (1200 mOsm/L to 50 mOsm/L)
        2. Appropriate central ADH release
          1. ADH is released in response to small increases in extracellular Sodium concentration
            1. Also released with volume depletion
          2. Inappropriately increased ADH release with SIADH
            1. Results in Isovolemic Hypoosmolar Hyponatremia
          3. Deficient ADH release occurs with Central Diabetes Insipidus
            1. Results in decreased collecting tubule permeability, water loss and Hypernatremia
        3. Appropriate renal ADH response
          1. ADH increases Medullary collecting tubule water permeability
            1. Water flows from the collecting tubule into the hypertonic Medullary interstitium
          2. Inappropriately increased ADH responsiveness with ADH-like drugs
            1. Results in SIADH
          3. Deficient ADH response occurs in Nephrogenic Diabetes Insipidus
            1. Results in decreased collecting tubule permeability, water loss and Hypernatremia
  • Physiology
  • Images
  1. Nephron
    1. nephron.png
  • References
  1. Marino (2014) ICU Book, p. 653-72
  2. Preston (2011) Acid-Base Fluids and Electrolytes, p. 3-30
  3. Rose (1989) Clinical Physiology of Acid-Base and Electrolyte Disorders, p. 3-27