Electrolyte balance in critically ill patients

1. WATER AND ELECTROLYTES
BALANCE
IN ICU
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO

2. Global Critical Care
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9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY

3. Objectives
• Explain in flow chart form how the rates
of sodium and water excretion are
affected by:
–Drinking isotonic saline
–Partial constriction of a single renal
artery
–Profuse sweating

4. Describe the effects of drinking water, or the intravenous
infusion of saline solutions of different osmolalities on the
volumes and osmolalities of various body fluid spaces.
EC vol. IC vol. EC osm. IC osm.
Isotonic saline
Water
Hypertonic Saline
Hypotonic saline

5. 1.
Sodium
Reabsorption

6. Sodium balance
Most NaCl intake added during food preparation
Sweat output depends on body temperature
Urine output of NaCl is regulated by blood pressure

7. Water balance
Metabolically produced by oxidation of H-containing nutrients
Insensible loss: expiration of 37 saturated air, evaporation through
skin (different from sweat)
Urine output regulated by vasopressin (antidiuretic hormone ADH)

8. Juxtaglomerular apparatus
Macula densa: specialized cells in wall of distal tubule
Juxtaglomerular cells (Granular cells): contain renin,
sympathetic nerves

9. Forces of filtration

10. Substance X: filtered & entirely secreted (rare)
Substance Y: filtered & partially reabsorbed (Na+, K+, water)
Substance Z: filtered & entirely reabsorbed (glucose, amino acids)
Kidney handling of various substances

11. Water Loading
Drink Water
Plasma Osmolality
Activation of osmoreceptors in
anterior hypothalamus
ADH secretion from Post. Pituitary
Water permeability in late DT and CT
Water Reabsorption
Urine Osmolality Urine Volume

12. Water
Deprivation Drink Water
Plasma Osmolality
Activation of osmoreceptors in
anterior hypothalamus
ADH secretion from Post. Pituitary
Water permeability in late DT and CT
Water Reabsorption
Urine Osmolality Urine Volume
4.

13. Review: Hormones of Water and
Sodium Regulation
• Angiotensin-II
• Anti-diuretic hormone/vasopressin/AVP
• Aldosterone
• Atrial natriuretic peptide (ANP)

15. Renin
angiotensin
aldosterone
system

16. Renin
angiotensin
aldosterone
system on
Na+
excretion

17. Macula densa: specialized cells in wall of distal tubule
Juxtaglomerular cells (Granular cells): contain renin, sympathetic
nerves
Juxtaglomerular apparatus
Mesangial cells.
1.
2.
3. Pressure (less stretch)
Decreased NaCl sensing
Sympathetic NS
RENIN

18. Actions of aldosterone
Aldosterone actions:  Na+ channel activity,  K+
channel activity,  Na+/K+ ATPase pump
Note: large Na+, K+ shows high concentration & vice versa

19. ANP actions:
1.  Na+ reabsorption from deep medullary collecting duct
2.  glomerular filtration rate
Both actions  Na+ excretion
Atrial
natriuretic
peptide on Na+
excretion

20. Vasopressin (ADH) release & actions
Vasopressin release stimulated by:
1.slight (1%) increase in plasma osmolality
2.large (~10-15%) reduction in plasma volume
Vasopressin action:
Increases permeability of collecting duct to
water

21. Vasopressin (ADH) release & actions
Renal medulla
has osmotic gradient from 300 mOsm/kg at
cortical border to 1200 mOsm/kg at deepest
part of medulla
 ADH levels  collecting duct
permeability  water reabsorption  urine
volume with  osmolality

22. Diabetes Insipidus
• Loss of ADH secretion or insensitivity of
kidneys to ADH
• Large severely dilute amounts of
urine
• Increased intake of water
• Danger lies in hyponatremia and ultimate
central nervous system edema and death.

23. Types of Diabetes Insipidus
• Central
– Damage to hypothalamus – no ADH
• Nephrogenic
– Kidneys cannot respond to ADH
– Usually genetic (rare) 90% cases due to V2
receptor mutation, 10% due to Aquaporin
mutation.

24. Types of Diabetes Insipidus
• Dipsogenic
–Damage to thirst center – making patient
abnormally thirsty
• Gestational
–During pregnancy women produce
vasopressinase which breaks down ADH,
increasing urine output.

25. ADH Mechanism of Action
Receptor binds, causes vesicles to fuse
and insert aquaporins (water channels)
into the membrane.
5.

26. How to test for it?
• Water deprivation test
– If water deprivation results in dilute voluminous
urine, then cause is likely not dipsogenic (but
central or nephrogenic)
• Desmopressin test (ADH analog)
– Central and Gestational respond to this treatment
– Nephrogenic does not
• If kidneys are insensitive, then they won’t respond.

27. SIADH
(syndrome of inappropriate ADH
secretion)
• Excessive ADH secretion
• Not “turned off” by drop in osmolality from
drinking water and water retention.
• Hyponatremia is also the main concern
• Causes
– Head trauma
– Ectopic lung tumor (secretes ADH).
– Treatment – water deprivation or removal of tumor

28. Water transport & vasopressin
actions

29. Sweat is hypotonic (i.e. osmolality <
plasma)
Sweating without
water
replacement

30. Regulation of thirst
Sensation of thirst stimulated by:
1. 1%  osmolality
2. >10-15%  blood volume
3.  angiotensin II

31. Isotonic saline
Extracellular volume
Blood pressure
Renin, angiotensin
aldosterone
Sympathetic NS
Sodium excretion
Plasma osmolality
Atrial Natriuretic peptide
ADH secretion
Water excretion
-

32. Extracellular fluid volume Extracellular osmolality
thirst ADH secretion
Water reabsorption
Water excretion
Sweating on salt & water excretion

33. Contstriction of renal artery
Afferent arteriole pressure
RENIN
Angiotensin-II
Aldosterone
Increase Na+
reabsorption
Plasma osmolality
vasoconstriction
ADH
Salt and water retention
Water excretion
Extracellular & vascular
volume
Increased systemic
blood pressure
GFR
Sodium filtered
Sodium excreted

34. What is renal hypertension? (renovascular hypertension)
BEFORE
AFTER
1) “ESSENTIAL” HYPERTENSION
-no specific cause
-body unable to regulate blood pressure
-systolic BP >140, diastolic > 90mmHg
-Managed with meds, diet, and fluid regulation
(ACE inhibitors/diuretics)
2) SECONDARY HYPERTENSION
-most common cause is
renal artery stenosis due to
atherosclerosis.
-usually diagnosed after long-standing
HTN becomes unmanageable.
-results in very high BP-systolic >200,
diastolic >100 mmHg.
-decreased RBF (sensed as a drop in BP) results
in increases in RENIN, thus causing further
peripheral vasoconstriction, sodium/water retention
and increases in BP.
PLAQUES OR
FIBROSIS

35. Isotonic expansion of renovascular
hypertension
Renin angiotensin aldosterone - high Both RVH and Aldosteronism result
in hypertension

36. AldosteroneCase E2
“hypertensive 43 y/o F”
Case E5
“nausea, weakness,
wt. loss 32 y/o M”
Tonicity TonicityVolume
Volume
[Na+] (144)
[K+] (2.9)
[Na+] (123)
[K+] (6.4)
HTN Bun/Cr = 26
Differentials
Isotonic Expansion
-hypertension
-renovascular hypertension
-aldosteronism
Hypotonic Contraction
-chronic salt loss w/water replac.
-diuretic use (chronic)
-Addison’s disease
Diagnosis Conn’s syndrome
Primary aldosteronism
(elevated Aldosterone/low renin)
Treatment/
Tests
Surgical removal of tumor
Spironolactone
Addison’s disease
(low Na, high K, acidosis,
low glucose, tanned appearance)
Measure [corticosteroid]

37. Excessive diuretic use (hypotonic contraction)?
Excessive loop or thiazide diuretic
↓ Na+ reabsorption DCT
↓ plasma osmolality
↓ ADH
↑ water excretion
↑ K+ excretion/
hypokalemia
(isotonic)
↓ vascular volume ↑ RAA
↑ Na reabsorption
(at principal cell)
↑ H excretion
Metabolic alkalosis
(when > 10%)
↑ ADH
↑ water retention
hyponatremia

38. Addison’s disease (hypotonic contraction)?
↓ aldosterone/glucocorticoids
↓ Na+ reabsorption (principal cell)
↓ plasma osmolality
↓ ADH
↑ water excretion
↓ K+ excretion/
hyperkalemia
(isotonic)
↓ vascular volume
↓ H+ excretion/
Metabolic acidosis
(when > 10%)
↑ ADH
↑ water retention
hyponatremia
(osmotic response)
hypoglycemia
(pressure response)

39. Anti-diuretic hormone
Case E3
“head trauma MVA”
Case E6
“SOB, wt. loss, hemoptysis
and wheezing”
Tonicity TonicityVolume Volume
[Na+] (162)
[K+] (3.8)
[Na+] (110)
[K+] (4.5)
Bun/Cr = 5.7
U[80]mOsmol
hemoconcentration
P[230]mOsmol
U[496]mOsmol
Differentials
Hypertonic Contraction
-dehydration – bun? Urine vol?
-acute renal failure – urine too dilute
-diabetes insipidus
Hypotonic Expansion
-polydipsia – [urine]?
-Addison’s disease
-SIADH
Diagnosis Diabetes Insipidus (low ADH)
High plasma osmolality,
Low urine osmolality
Treatment/
Tests
Desmopressin test
(response – neurogenic)
(no response – nephrogenic)
SIADH (high ADH)
Low plasma osmolality
High urine osmolality
Chest X-ray
Remove ADH secreting tumor
water loss > salt loss salt loss > water loss

40. SIADH (hypotonic expansion) vs. Diabetes Insipidus (hypertonic contraction)
↑ Anti-diuretic hormone ↓
↑ thirst – activation of
hypothalamic
osmoreceptors
↓ Na reabsorption
↓ K excretion
↓ renin-angiotensin-
aldosterone
↑ MAP
↑ water reabsorption
at principal cells
↑ vascular volume
↑ water excretion
↓ MAP
↓ vascular volume
hyponatremia
Water retention + Na excretion explains low plasma osmolality
and relatively increased urine osmolality (SIADH)
↑ ANP
↑ renin-angiotensin
aldosterone
↑ Na reabsorption
↑ K excretionhypernatremia

41. Global Critical Care
https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY

42. GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com