Regulation of Sodium Balance Flashcards
Revised Henderson eqn
pH = 24 x (pCO2/HCO3)
but this needs to be converted to [H+]
What is the relationship between pH and [H+]?
at pH of 7.4, [H+]= 40
change of pH of 0.3= 2x[H+]
- 7=20
- 1=80
- 8=160
There are no specific “normal” values for urinary concentrations. Why?
Plasma constituents of water and numerous solutes are maintained within a very narrow range by the homeostatic mechanisms performed by the kidney. This requires variation in the urinary excretion of water and solutes by the kidney.
Normal plasma concentrations:
Arterial blood gas measurements:
Sodium 140 meq/l pH 7.40
Potassium 4.0 – 5.0 meq/l CO2 40 mm Hg
Chloride 104 meq/l
Bicarbonate 24 meq/l
BUN 10 mg/dl
Creatinine 1.0 mg/dl
Calcium 9.0-10.0 mg/dl
Phosphorus 4.0–5.0 mg/dl
Albumin 4.0-4.5 g/dl
Osmolality ~290 mosm/kg H2O
TBW represents what percentage of BW?
60%
2/3 of TBW is intracellular fluid volume (ICFV).
ICFV = 0.4 BW
1/3 of TBW is extracellular fluid volume (ECFV). ECFV = 0.2 BW
3/4 of ECFV is interstitial fluid volume (ISFV). ISFV = 0.15 BW
1/4 of ECFV is plasma volume (PV). PV = 0.05 BW
T or F. ICFV osmolality always equals ECFV osmolality
T, due to passive movement of H20
What is the major cation in ICFV? ECFV?
K+. Na+ is major cation of ECFV since it is virtually restricted to ECFV.
What are the events that follow the ingestion of Na+?
- increased TBNa
- increased osmolarity of ECFV since Na+ is restricted
- leading to increased thirst and H2O intake and AVP secretion
So what is the net result of ingestion of Na+?
The net result then is retention of isotonic NaCl and expansion of ECFV with little or no change in ICFV.
How is isotonic volume depletion performed?
Isotonic volume depletion occurs when isotonic fluids are lost from the ECFV such is the case in vomiting of gastric contents or diarrhea
What is the result on ICFV of isotonic volume depletion?
no change in ICFV since ECFV osmolality is unchanged because the volume lost is isotonic
The composition of ions in gastric and intestinal fluid differ from plasma. How would vomiting (loss of gastric fluid) affect the body?
Gastric losses are rich in HCl and would, therefore, be associated with metabolic alkalosis in addition to the ECFV loss.
How would diarrhea (loss of intestinal fluid) affect the body?
Intestinal fluid is relatively rich in HCO3- and would result in normal anion gap metabolic acidosis in addition to ECFV loss.
NOTE: Changes in TBNa (up or down) are synonomous with changes in ECFV
increased TBNa lead to ECFV expansion and decreased TBNa leads to ECFV depletion
Plasma Na+ concentration (mEq/L) per se tells you nothing about TBNa content or the size of the ECFV. Why?
Plasma Na+ concentration is always determined by the ratio of TBNa to TBW (more specifically to ratio of total body cations to total body water, K in ICFV and Na in ECFV)
Low plasma Na+ concentration could be associated with low, normal, or expanded ECFV depending on the relative changes in TBNa, TBW, or both. The same would be true for increased Na+ concentration.
A 65 yo women with a weight of 60kg has x L in the extracellular compartment. What is the value of x?
10L
TBW= 0.5BW in a woman
and = 0.6BW in a man
and ECF is 1/3 of TBW
A 28 yo women with no other medical problems comes to the ED with nausea and diarrhea. Her lying down BP is 100/70 and on standing drops to 80/60. She is tachycardia with cool extremities. Which set of urine electrolytes would you find in this patient?
urine Na mEq/L Uosm A. 5 100 B. 75 900 C. 5 900 D. 75 100
C. Whenever there is extra-renal loss of sodium and the kidneys are normal, the kidneys will work to conserve Na and water
What happens to water balance after ingestion of a water load?
Reduction in Posm with low ADH and a dilute urine
Where is most of the plasma volume distributed?
80% venous and 20% arterial
A. A 56 yo woman with type 2 diabetes mellitus, HTN. and CAD presents to the ED with chest pain and SOB. Her physical exam is significant for JVD, S3 gallop, bilateral rales (fluid in alveoli) and lower extremity edema.
Na 130 mEq/l, K 4.2mEq/L, Cl 89mEq/L, HCO3- 24mEq/L, serum creatinine is 1.5mg/dl, glucose is 120mg/dL
What will happen? (ECFV= extracellular fluid volume, ECV= effectives circulating volume)
Her ECFV is expanded, CO is low, and ECV is reduced
Notice here that the total body Na+ is elevated even though serum Na+ is decreased (so this patient is hypoatremic)
Total body Na+ is synonomous with ____.
ECFV. Is NOT the same as serum Na+. Can tell it’s elevated by a clinical exam that is similar to CHF (extended EJV, edema, bilateral rales etc.)
What are the major constituents of ECF?
Na+, Cl-, and HCO3-
What happens when the body feels that ECV is low?
Afferent sensors such as renin, catecholamine, thirst, and ADH are increased and ANP is decreased leading to Na+ and water retention
What are the roles of angio II?
- Vasoconstriction
- increases PT reabsorption of Na+ (Thus, urine Na+ decreases)
What are the roles of aldosterone?
-increases distal reabsorption of Na+
Thus, urine Na+ decreases
What does ADH result in?
distal collecting tube becomes permeable to water for increased reabsorption (making the urine more concentrated- i.e. Uosm will increase)
What is ECV?
relates to the fullness and tension within the arterial tree Because only 15% of total blood volume is in the arterial compartment, arterial blood volume can be decreased in elation to the holding capacity of the tree.
What are some situations where ECV is decreased in the presence of an elevated ECVF?
- CHF
- liver disease
- sepsis
- nephrotic syndrome
- pregnancy
- anaphylaxis
Why would liver disease be associated with a decrease in ECV in the presence of an elevated ECVF?
Because a lot of the blood is pooled into the splanchnic circulation
When volume depletion occurs due to extra renal losses (e.g. diarrhea, burns) with normal renal function, how does the urine present?
urine becomes highly concentrated and salt poor
When volume depletion occurs due to renal losses (e.g. diuretics), how does the urine present?
urine in inappropriate dilute and sometimes rich in salt
What are some clinical features of volume depletion?
- hypotension
- poor skin turgor
- cool extremities
How does the body react to balance water upon increase in ECF osmolality?
-CNS osmoreceptors are activated (after only 2% increase in osmolality) and release ADH release (this is called osmotic ADH release) causing water retention (as well as angio II)
How does the body react to balance water upon decrease in effective circulating volume?
A decrease in 7-10% of effective circulating volume causes baroreceptor release of ADH (this is called non-osmotic ADH release) and angio II stimulating volume retention
What is the eqn. for serum Na+ conc.?
Na(TBNa)/water volume (TBW)
most causes of hypoatremia are caused by a relative increase in TB water
What is hypoatremia defined as?
An abnormally low plasma Na+ conc. (less than 135mEq/L)
diagnosis can be made from lab values
If you see that the patient has hypoatremia, then what should you do next?
check osmolality (most will be hypo-osmolar due to the significance of [Na] in the plasma osmolality formula)
What things can cause a hyperosmolar hypoatremia?
- mannitol is hyper-osmolar so it drags out water from the ICF to cause hypoatremia
- hyperglycemia
What should you do next once you know a patient has a hypo-osmolar hypoatremia?
is the ECVF elevated or lowered
A 78yo man is brought into the ED fro decreased appetite and ‘altered mental statue’. On exam he is responsive to strong stimuli, has dry mucous membranes, flat neck veins, sacral decubitus ulcers and appears to be moving all extremities and facial muscles without deficits. Vital T=97.0, BP=80/50, HR=130, RR-14.
Na=121, K=4.5, Cl=9.5, HCO3-=32, Glucose=140
What are the changes in TBW and TBNa in this patient compared to baseline?
TBW and TBNa are both decreased but TBNa is lost more, but ADH has been activated
Know TBNa is decreased from clinical signs
This is hypovolemic hypoatremia- hypovolemic based on clinical signs and hypoatremic based on labs
Describe hypovolemic hypoatremia
sodium depletion with reduction in ECF volume and secondary water retention due to non-osmotic stimulation of AVpPrelease
Thus, TBW decreases and TBNa decreases even more translating to excess TB water relative to TBNa
A 78yo women was brought to the hospital after a fall. Has Hx of HTN for which she took a CCB. A selective SSRI streamline has been prescribed 2 months prior for depression. She reported climbing a flight of stairs when she fell. Before the fall she experienced thirst for a number of days, but did not report other complaints. On exam, she had several cranial bruises, was disoriented to time and place. BP: 120/90, pulse of 80. No apparent sings of extracellular fluid volume contraction (so TBNa+ is normal)
Na 125 (low), K 4.2, Creatinine 0.8mg/dL, serum osmolality 255mOsm/kg (low), Urine Na=44 mEq/L, urine Osml=523 mOsm/kg
she has hypo-osmolar euvolemic hypoatremia
So her TBNa+ is normal and TBwater must be elevated
In this, ADH should shut off and the Uosm should decrease (dilute-less than 100) but here her Uosm is way too high suggesting that she is retaining fluid because she has elevated ADH causing inappropriately concentrated urine
Describe euvolemic hypoatremia.
water retention due to autonomous or altered regulation of vasopressin release (common cause- SIADH) causing increased TBwater and normal TBNa
Causes of euvolemic hypoatremia?
- pulmonary disorders, CNS disorders, cancers
- vasopressin analouges
- hypothyroidism
What are some vasopressin analouges?
chlorpropamide, clofibrate, narcotics, narcotics, carbemezepine, antipsychotics
A 44yo patient with cirrhosis of the liver comes in with SOB. Exam revealed BP 100/70, elevated JVD, ascites, and marked pedal edema.
Na-126 Meq/L, K 4.2 mEq/L
Cl 90, HCO3 28, BUN 20
urine Na 10 and urine osmolality is 800mOsm/kg
Why is her serum Na so low?
hypo-osmolar hypervolemic hypoatremia
Non-osmotic stimulation of vasopressin release because of reduced ECV
Causes of hypervolemic hypoatremia?
- CHF
- Hepatic cirrhosis
- Nephrotic syndrome
- Renal disease
A 75yo female NH resident is brought to the ED because of altered mental statue. She has stopped drinking after developing diarrhea due to trial gastroenteritis. She is found to communicate poorly. Brief physical exam reveals diminished skin turgor and flat neck veins. BP is 80/60. pulse 120, RR 20. Serum sodium 168, urine Na is 10, and Uosm is 600 mOsm/kg
Whats going on?
She has external losses of sodium that are exceed by loss of free water
Physical exam shows that TBNa is low, and thus the kidneys are conserving the Na and water via ADH
This hypovolemic hypernatremia
Does the presence of ADH makes the urine dilute or concentrated?
concentrated
T or F. Hypernatremia is usually caused by excess water loss rather than sodium gain
T. Usually develops in those who cant sense thirst properly or in ADH resistance
45 yo WM comes after head injury. She has polyuria (U/O 10L/day). She is confused. BP is normal and she has no edema. Sr. Na is 165 Sr ism 330 Uosm is 70. She is treated with dDAVP nasal spray and within 24 hrs her Sr Osm drops to 295. and urine ism increased to 620. What’s going on here?
She has absence of AVP
central is when you have no ADH, and nephrogenic is when you have ADH but its not working for some reason
So this person must have central because treatment worked
