1. Na /K Disorders
Dr Mojgan Mortazavi

2. SODIUM

4. Hyponatremia

5. Hyponatremia
Hyponatremia defined as a Na+ <135meq/l that usually reflects hypoosmolality.
Low plasma osmolality causes water movement into the cells and then cellular overhydration particularly in brain cells

6. Symptoms of hyponatremia
The changes induced by acute hyponatremia (developing over 1-3 days) may result in permanent neurological damage and are primarily duo to cerebral overhydration
Nausea and malaise as the plasma Na+ falls acutely below 125 meq/l
Headache, lethargy, and obtundation may appear in Na+ between

7. Symptoms of hyponatremia…..
The more sever changes of seizures and coma are not seen until the plasma Na+ is less than meq/l
Women particularly premenopausal women ,appear to be at much greater risk of developing sever neurologic symptoms and of irreversible neurologic damage than men that may be related to differences in cerebral metabolism and sex hormones.

9. Treatment
There are two basic principles involved in the treatment of hyponatremia: rasing the plasma Na+ at a safe rate treating the underlying cause

10. Treatment with Nacl True volume depletion Diuretics
Adrenal insufficiency

11. Treatment with H2O restriction
SIADH
Edematous state
Renal failure
Primary polydipsia

12. The risk factors for developing osmotic demyelination
1-More than a 12 meq/l elevation in Na+ in the first day
2-Over correction of the Na+ to above 140 meq/l within the first 2 days
3-Hypoxic or anoxic episodes prior to therapy

13. TREATMENT OF SIADH Acute: 1-water restriction
2-hypertonic saline or Nacl tablets
3-loop diuretics
Chronic:
2-high salt ,high-protein diet
3-loop diuretic
4-demeclocycline ,lithium

14. TREATMENT OF SIADH Asypmtomatic or Chronic SIADH Water restriction
0.5-1 liter/day
Salt tablets
Demeclocycline
Inhibits the effects of ADH
Onset of action may require up to one week

15. Treatment Goal: raise Na by <10 meq/L in the 1st 24 hours

16. Central Pontine Myelinosis
Correction of Na too FAST
more common w/alcoholism, malnutrition, chronic illness
Symptoms: flaccid paralysis, dysarthria, dysphagia
Evolve over days – weeks
May extend dorsally  Sensory Tracts
locked-in syndrome
Turn off ADH & prompt diuresis 
Sudden & Dramatic Inc serum Na

18. Hyponatremia Example: Answer:
a 60 kg women with a plasma sodium of 110 meq/L
Formula:
ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
What is the TBW?
How high will 1 liter of normal saline raise the plasma sodium?
Answer:
TBW is 30 L
Serum sodium will increase by approximately 1.4 meq/L for a total SNa of meq/L

19. Hyponatremia Example: Answer:
a 90 kg man with a plasma sodium of 110 meq/L
Formula:
ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
What is the TBW?
How high will 1 liter of 3% saline raise the plasma sodium?
Answer:
TBW is 54 L
Serum sodium will increase by approximately 7.3 meq/L for a total SNa of meq/L

20. Hyponatremia Example:
63 y/o female at 75 Kg with N/V/D for 4 days
SNa is 108 mEq/L
She has had one seizure in the ambulance
Plasma osmolality is 251 mosmol/kg
Urine osmolality is 47 mosmol/kg
Uric acid is 6mg/dl
What type of hyponatremia does this patient have?
What additional labs/studies would you want?
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21. Hyponatremia How will you Tx her? Calculate the total body water
0.5 x weight = 37.5 L
What rate of correction do you want?
8 to 10 mEq/L in 6 to 8 hours
What fluid will you use?
3% Saline
How will you calculate the amount of sodium to give her?
ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
How will her sodium increase after 1 liter of 3% saline?
By 10.8 mEq/L to mEq/L

22. Hyponatremia What other medication will she need?
Lasix and a foley
Her sodium increases to mEq/L over the next 8-10 hours. How will you continue to correct her hyponatremia?
ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
ΔSNa = 154mEq/L – 118.8mEq/L ÷ 38.5L = 0.9 mEq/L
So 2 liters of normal saline over the next 14 hours

23. Hypernatremia

24. HYPERNATREMIA Hypernatremia is defined as a plasma Na+>145 meq/l
Hypernatremia represent hyperosmolality that results in water movement out of the cells into the extracellular fluid that causes cellular dehydration in the brain that is primarily responsible for the neurologic symptoms.

25. Generation of hypernatremia
Water loss: hypernatremia due to water loss occurs only in patients who have hypodipsia, in adults with altered mental status, and in infants.
Na+ concentration > 150 is virtually never seen in an alert adult with a normal thirst mechanism and access to water.

26. Fluid volume status assessed by physical eaxam
Hypernatremia
Fluid volume status assessed by physical eaxam
Hypovolemic
Loss of H2O>Na+ loss
Isovolemic
Loss of H2O
Hypervolemic
Gain H2O and Na+
Check urine Na+
Check urine Na+
Check urine Na+
>20 mEq/L
<10 mEq/L
>20 mEq/L
Renal loss
Diuretic
Glycosuria
Renal failure
Extrarenal loss
GI-vomiting
GI-diarrhea
Excess
sweating
Respiratory loss
Renal loss
Diabetic insipidis
Central
Nephrogenic
Extrarenal loss
Insensible losses
Skin
Respiration
Iatrogenic
Hypertonic NaHCO3
NaCl tablets
Hypertonic solutions
Mineralocorticoid
1 Hyperaldosteronism
Cushing disease
Adrenal o
Hypertonicdialysis
Hemodilysis
Peritoneal dialysis
Treatment
Water replacement
D5W at 1-2 mEq/L/hr
± vasopressin for
Central DI
Treatment
Saline then hypotonic
solution
Treatment
Diuretics ± dialysis

27. Symptoms of hypernatremia
Lethargy ,weakness, irritability, are the earliest findings which can then progress to twitching ,seizures, coma, and death that are more related to cellular dehydration in the brain.
Patients with chronic hypernatremia may be relatively asymptomatic despite a plasma Na+ >170
The severity of the neurologic symptoms is related to the both the degree and more importantly ,the rate of rise in the effective plasma osmolality.

28. Treatment of hypernatremia
Rapid correction of hypernatremia can induce cerebral edema, seizures, permanent neurologic damage, and death therefore the plasma Na+ must be slowly lowered unless the patient has symptomatic hypernatremia.

29. Treatment of hypernatremia……
Water deficit= LBW( plasma Na-140/ 140)
The maximum safe rate at which the plasma Na+ should be lowered (in the absence of hypernatremic symptoms) is 0.5 meq/L/h or 12 meq/L/per day

30. Formula for Managing Hypernatremia
CLINICAL USE
Estimate the effect of 1 liter of any infusate on serum Na+
Estimate the effect of 1 liter of any infusate containing Na+ and K+ on serum Na+
FORMULA*
1. Change in serum Na+ =
2. Change in serum Na+ =
infusate Na+ - serum Na+
total body water + 1
(infusate Na+ + infusate K+) -serum Na+

31. Characteristics of Infusate
Infusate Na+
Extracellular-Fluid Distribution
mmol per liter %
5% Dextrose in H20 40
0.2% NaCl in 5% dextrose in H2O 34 55
0.45% NaCl in H2O 77 73
Ringer’s lactate
130 97
0.9% NaCl in H2O
154
100

32. Summary of Managing Hypernatremia
Isotonic saline unsuitable except in ECF volume depletion causing hemodynamic instability
Switch to hypotonic solutions as soon as circulatory status stabilized
Avoid excessive rapid correction or over correction
Select the most hypotonic infusate suitable with appropriate allowances for ongoing fluid losses
Most important - reassess infusion prescriptions at regular intervals based on pt’s clinical status and electrolyte values

34. POTASSIUM

36. POTASSIUM BALANCE
Potassium is the major intracellular cation that is essential for a variety of cellular and neuromuscular functions.
The total body K+ stores in a normal adult are meq(50-55meq/kg) and the normal plasma concentration is meq/l and inside cells is about 140 meq/l

37. Regulation of potassium balance
The maintenance of K+ balance involves two functions: the normal distribution of K+ between the cells and extra cellular fluid the renal excretion of the K+ added to the extra cellular fluid from dietary intake and endogenous cellular breakdown

38. Factors influencing the distribution of K+ between the cells and extra cellular fluid
Physiologic:
1-Na+k+ ATPase
2-catecholamines
3-insulin
4-plasma potassium concentration
5-exercise
Pathologic:
1-chronic disease
2-extra cellular PH
3-hyperosmolality

39. Renal excretion of k+
The urine is major route by which the K+ derived from diet and endogenous cellular breakdown , is eliminated from the body.
The primary event in urinary K+ excretion is the SECRETION of K+ from the tubular cell in to the lumen in the distal nephron.

40. Renal Handling of K+ Glomerulus: freely filtered
PCT, Thick As limb LOH : reabsorbed

41. Hypokalemia

42. Hypokalemia
Hypokalemia is defined as a K+ <3.5 meq/l, may result from one or more of the following: decreased net intake
2-shift into the cells
3-increased net loss

44. Hypokalemia
Exclude reredistribution
Alkalosis
Insulin
Periodic paralysis
Barium poisoning
Vitamin B12 therapy
Extrarenal K losses
Urine electrolytes
K+<20 mEq/day
Na+>100 mEq/day
(If Na+<100 mEq/day repeat
Test after increasing dietary
Na+>100 mEq/day)
Biliary losses
Lower GI losses
Fistula
Skin losses
Renal K losses
Urine electrolytes
K+>20 mEq/day
Na+>100 mEq/day
High blood pressure
Normal blood pressure
Plasma renin levels
Serum HCO3 -

45. Plasma renin levels
Serum HCO3 -
High plasma renin
Malignant HTN
Renovascular disease
Renin secreting tumor
Low plasma renin
Low HCO3 –
RTA
High HCO3 -
Aldoserone
Urine chloride
High
Hyperlado-
Steronism
Bilateral
hyperplasia
Low
Mineralocorticoid
Ingestion
Adrenal hyperpasia
(congenital)
Cushing syndrome
Serum K+
(mEq/L)
<10 mEq/day
Vomiting
<10 mEq/day
Bartter
Syndrome
Diuretics
Magnesium
deficiency
Normal 4
Normal
T U
Low T wave
High U wave 3
Hypokalemia
T U
Inverted T wave
High U wave
Low ST segment
3.5

46. Symptoms of hypokalemia
Marked symptoms are unusual unless the plasma K+ concentration is below meq/l ,but in susceptible patients even mild reductions in the plasma potassium can predispose to potential fatal arrhythmia.

47. Clinical Features Hypokalemia < 3 mEq/L : Symptomatic
Mild hypokalemia : generally asymptomatic
Increased risk of mortality for pts with cardiovascular disease – trigger ventricular tachycardia / ventricular fibrillation
(decrease K+ : d/t sympathetic stimulation)
Digitalis induced arrhythmias – can occur with normal drug levels if hypokalemia is present
Diuretic induced hypokalemia & hypomagnesemia must be avoided in pts on drugs that prolong QT interval : as it predisposes to polymorphic VT / Torsade de pointes
Hypokalemia < 3 mEq/L : Symptomatic

48. Cardiac Digitalis Intoxication : ventricular extrasystoles
ventricular tachycardia
ventricular fibrillation
partial-complete AV block
bradycardia
atrial flutter
atrial fibrillation
Ventricular arrhythmias : tachycardia / fibrillation

49. Neuro-muscular Fatigue Myalgia Muscular weakness involving lower limbs
Severe Hypokalemia :
Paralysis ( extremities )
Weakness of respiratory muscles ( dyspnea )
Rhabdomyolysis (exercise induced)

50. Gastro-intestinal
Constipation
Paralytic ileus

51. Fluid – Electrolyte Polyuria ( nephrogenic diabetes insipidus )
Polydipsia ( nephrogenic diabetes insipidus )
Increased ammonia production ( intracellular acidosis ) precipitate hepatic coma in pts with advanced liver ds
Edema
Chloride wasting
Metabolic alkalosis
Hypercalciuria
Phosphaturia

52. Endocrine Glucose intolerance ( decreased insulin secretion )
Growth retardation ( Reduced Growth hormone receptors
Reduced IGF-1 )

53. Hemodynamic
Hypertension ( increased renin secretion )

54. Abnormalities induced by hypokalemia
Muscle weakness or paralysis
Cardiac arrhythmias
Rhabdomyolysis
Renal dysfunction impaired concentrating ability increased ammonia production impaired urinary acidification increased bicarbonate reabsorption renal insufficiency
Hyperglycemia

55. Basic Investigations ECG : Initially : flattening of t wave
depression of ST Segment
development of prominent u waves
Severe hypokalemia : increased amplitude of p wave
increased QRS duration
S.Potassium

57. Treatment of hypokalemia
Monitoring of ECG and muscle strength, is an essential part of the management of patients with sever hypokalemia
There is no definite correlation between the PLASMA k+ and BODY K+ stores.
A reduction in the plasma K+ from 4 to 3 meq/l requires the loss of meq of K+

58. Renal Vs Extra renal loss
Urinary K+: > 20 mEq/L – Renal loss
Urinary K + : < 20 mEq/L – Extrarenal loss
TTKG : Transtubular Potassium Gradient
( Urine K+ / Plasma K+ )
( Urine Osm / Plasma Osm )
TTKG : Renal loss : > 4
Extra renal loss : < 4

59. Extra Renal Loss Urinary K+ < 20 mEq/L Metabolic Acidosis Normal pH
GI Loss
Diarrhoea
Laxative Abuse
Normal pH
Villous Adenoma
Geophagia
Metabolic Alkalosis
Laxative abuse : rare
GI Loss: rare

60. Renal Loss Urinary loss K+ > 20 mEq/L Metabolic Acidosis
RTA
DKA
Ureterosigmoidostomy
Variable pH
ATN recovery
Post obstructive diuresis
Drugs
Metabolic Alkalosis
Urinary chloride level

61. Renal loss - Drugs Amphotericin B : tubular damage
increased excretion of K+
Aminoglycosides : renal wasting of K+
Thiazides, Furosemide, Acetazolamide : renal loss K+
Cisplatin
HYPOMAGNESEMIA : Significant renal K+ wasting

62. Renal Loss + Metabolic Alkalosis
Urinary Chloride
< 20 mEq/L
Vomiting
Diuretics
> 20 mEq/L
Check BP

63. Renal loss +Urine Cl > 20 mEq/L
Check BP,ECF
Low BP
Check Bicarb
Low - RTA
High : Bartter, Gitelman
HTN , Increased ECF
Check Renin, Aldosterone

64. Treatment of hypokalemia…….
A variety of potassium preparations are available for oral and IV use including the CL-, HCO3-, phosphate ,gluconate.
In metabolic alkalosis and hypokalemia KCL preparation is choice
In metabolic acidosis and mild degree of hypokalemia KHCO3 is preferred
ORAL: KCL can be given orally in salt substitutes as a liquid or in a slow release tablet or capsule

65. Treatment of hypokalemia…….
IV: the standard IV kcl solution contains 2meq/ml each of k+ and cl-.
20-40 meq of k+(10-20 ml) is added to each liter of saline solution.
In general ,no more than 60 meq/l should be given through a peripheral vein ,since higher concentration of k+ are very irritating ,resulting in pain and sclerosis of the vein.

66. Treatment of hypokalemia……..
1-If k+ is between 3 to 3.5 meq/l treatment is not urgent and these patients can usually be treated with oral kcl at an initial dose of meq/day
2-In patients with sever symptoms or marked hypokalemia ,k+ must be give more rapidly The plasma k+ will acutely rise by as much as meq/l after meq oral kcl and by meq/l after meq/l but these maximum effect is transient ,why?

67. Rate of potassium repletion
IV potassium is administered at a maximum rate of meq/h although as much as meq/h has been given to patients with paralysis or life threatening arrhythmias.
This solution containing as much as 200 meq of k+ /L and are best tolerated if given into a large vein such as femoral vein (infusion through a central venous line should probably be avoided, why?

68. Rapid administration of k+ is potentially dangerous even in severely k+ depleted patients and should be used only in life threatening situation

69. HYPERKALEMIA

70. HYPERKALEMIA
Hyperkalemia defined as a k+>5meq/l occurs as a result of either k+ release from cells or decreased renal loss.
There is an adaptive response in hyperkalemia

71. Hyperkalemia
Spurious
Hemolysis
Thrombocytosis
Leukocytosis
Mononucleosis
(leaky RBC)
Redistribution
Acidosis
Diabetic ketoacidosis
β-Blockade
Succinylcholine
Periodic paralysis
Digoxin toxicity
Potassium excess
Increased intake/
tissue release
Interavenous/oral intake
Hemolysis
Rhabdomyolysis
Tumor lysis
Stored blood
Renal function
Serum K+
(mEq/L)
Atrial standstill
Intraventricular
block
GFR >20 mL/min
GFR <20 mL/min
Acute renal failure
Chronic renal failure 9
Hyperkalemia 7
Aldosterone Deficient
Addison disease
Hereditary
Adrenal defects
Drugs
Heparin
NSAID
ACE inhibitors
Cyclosporine
spironolactone
Tubular hyperkalemia
Without aldosterone
Deficient
Acquired
Obstruction
Renal transplants
SLE
Amyloidosis
Sickle cell
Drugs
K-sparing diuretics
High T wave
Normal 4
Normal

72. Symptoms of hyperkalemia
1-Muscle weakness : most often begins in the lower extremities and ascends to the trunk and upper extremities *The respiratory muscles and those supplied by the cranial nerves are usually spared
2-Abnormal cardiac conduction: the cardiac toxicity is enhanced by hypocalcemia, hyponatremia, acidemia, and a rapid elevation in the plasma k+ concentration

73. EKG Changes Peaked T Waves

75. EKG Changes Widening of QRS Complex

76. EKG Changes Ventricular Tach/Torsades

77. Treatment of hyperkalemia
Emergency
Modality
Mechanism of action
Onset
Duration
Prescription
K+ Removed
From Body
Calcium
Antagonizes cardiac
Conduction abnor-
malities
0-5 minutes
1 hour
Calcium gluconate
10%,5-30 mL IV;
Or calcium chloride
5%,5-30 mL IV
Bicarbonate
Distributes K+ into
cells
15-30 minutes
1-2 hours
NaHCO3,
44-88 meq
(1-2 ampules) IV
Insulin
15-60 minutes
4-6 hours
Regular insulin,
5-10 units IV,plus
glucose 50%,25 g
(1 ampule) IV
Albuterol
2-4 hours
Nebulized albuterol,
10-20 mg in 4 mL
normal saline,in
Haled over 10 minutes

78. No emergency Modality Mechanism of action Duration of Treatment
Prescription
K+ removed
From body
Loop diuretic
Renal K+ excreation
0.5-2 hours
Furosemide,40-160
mg IV or orally with
Or without NaHCO3,
0.5-3 meq/ kg daily
Variable
Sodium polystyrene
Sulfonate
(kayexalate)
Lon exchange resin
binds K+
1-3 hours
Oral: g in 20%
Sorbitol ( mL)
Rectal: 50 g in 20%
sorbitol
0.5-1 meq/q
Hemodialysis
Extracorporeal K+
removal
48 hours
Blood flow ≥ 200-
300 mL/min,
Dialysate [K+] ~ 0
meq
Peritoneal dialysis
Peritoneal K+ removal
Fast exchange ,
3-4 L/h