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Electrolytes
Disturbances
DR/ Shafiq .A. Al-imad
Hypokalemia
Definition
 Total body K : 3500 mmole(98%
intracellular, 2% extracellular)
 Normal serum potassium 3.5-5.5 mEq/L
 Hypokalemia is a serum potassium less
than 3.5 mEq/L
 American diet : 100 mmole
 Haemostasis system of K :
 1) kidney , intestine
 2) Shifting of K between the ECF and
ICF
Blood pressure
Blood pressure
Renin
Renin
Renin
Renin
Aldo
Aldo
K
K+
+
excretion rate and acid
excretion rate and acid-
-
base status ?
base status ?
H
H
H
Hy
y
y
yp
p
p
po
o
o
ok
k
k
ka
a
a
al
l
l
le
e
e
em
m
m
mi
i
i
ia
a
a
a &
&
&
& P
P
P
Pa
a
a
ar
r
r
ra
a
a
al
l
l
ly
y
y
ys
s
s
si
i
i
is
s
s
s
L
L
L
Lo
o
o
ow
w
w
w K
K
K
K+
+
+
+
e
e
e
ex
x
x
xc
c
c
cr
r
r
re
e
e
et
t
t
t i
i
i
io
o
o
on
n
n
n a
a
a
an
n
n
nd
d
d
d
n
n
n
no
o
o
or
r
r
r m
m
m
ma
a
a
al
l
l
l a
a
a
ac
c
c
ci
i
i
id
d
d
d-
-
-
-b
b
b
ba
a
a
as
s
s
se
e
e
e



SPP
SPP



Barium poisoni
Barium poisoning
ng



FPP
FPP 


Hypernatremic HPP
Hypernatremic HPP
None
None Family history
Family history Hypernatremia
Hypernatremia
High K
High K+
+
excretion and
excretion and
abnormal acid
abnormal acid-
-base
base
Acid
Acid-
-
base state ?
base state ?
Clue
Clue
Hyperthyroidism ?
Hyperthyroidism ?



TPP
TPP
YES
YES NO
NO Metabolic Acidosis
Metabolic Acidosis
NH
NH+
+
4
4 excretion
excretion
(UAG, UOG)
(UAG, UOG)
Low
Low
High
High
Toluene
Toluene
Profound diarrhea
Profound diarrhea
RTA
RTA
Metabolic Alkalosis
Metabolic Alkalosis
R
Renin
enin
Normal
Normal
GS or BS
GS or BS
Diuretics
Diuretics
Vomiting
Vomiting
High
High
Primary
Primary
mineralocorticoid excess
mineralocorticoid excess
Aldo
Aldo
Aldo
Aldo
Primary
Primary
Aldo
Aldosteronism
steronism
Licorice use
Licorice use
AME
AME
Ectopic ACTH
Ectopic ACTH
Liddle syndrome
Liddle syndrome
Lin SH et al. Am J Emerg Med 2003 (
Lin SH et al. Am J Emerg Med 2003 (
electro                           lyte.ppt
 Case 1
A 43 yo male patient with HTN has been on atenolol
and HCTZ was found to have a serum K+ 3.2 meq/L.
 Case 2
A 55 yo diabetic female was admitted to the ICU with
severe vomiting, diarrhea and muscle weakness,
initial work up revealed serum K+ 2.1 meq/L.
Symptoms
Mild to moderate hypokalemia
 3 and 3.5 meq/L; this degree of
potassium depletion usually produces
no symptoms, except for
 patients with heart disease ( taking digitalis
or undergoing cardiac surgery or
 advanced cirrhosis.
Treatment of mild to moderate
hypokalemia
 . In general, the loss of 200 to 400 meq
of potassium is required to lower the
plasma potassium concentration from
4.0 to 3.0 meq/L
 Repletion as oral potassium chloride in
divided doses over few days
 Treat the underlying cause
Treatment of mild to moderate
hypokalemia
For patients who can’t tolerate oral KCL
 I.V KCL where 20 to 40 meq of
potassium is added to each liter of fluid.
A saline rather than a dextrose solution
is preferred for initial therapy, since the
administration of dextrose can lead to a
transient 0.2 to 1.4 meq/L reduction in
the plasma potassium concentration
SEVERE HYPOKALEMIA
Symptoms
 Muscle weakness and paralysis
 Renal dysfunction
 ECG changes and arrhythmias
ECG changes
 depression of the ST segment,
 decrease in the amplitude of the T wave,
and
 increase in the amplitude of U waves
which occur at the end of the T wave. U
waves are often seen in the lateral
precordial leads V4-V6.
electro                           lyte.ppt
Treatment of severe
hypokalemia
 . A patient with a plasma potassium
concentration of 2 meq/L, for example, may
have a 400 to 800 meq potassium deficit
 The maximum rate of intravenous potassium
administration is 10(peripheral line) to
20(central line) meq/h, although higher rates
have been given to selected patients with
paralysis or life-threatening arrhythmias
Treatment of severe
hypokalemia
 In this setting, solutions containing as
much as 200 meq of potassium per liter
(20 meq in 100 mL of isotonic saline)
have been used. These solutions
should be infused into a large vein
( femoral vein, subclavian vein, or
internal jugular vein)
Treatment of severe
hypokalemia
 Accidental administration of very large
quantities of intravenous potassium can
be avoided by limiting the amount of
potassium per container (eg, 20 meq in
100 mL of isotonic saline)
Treatment of severe
hypokalemia
 Careful monitoring of the physiologic effects
of severe hypokalemia (ECG abnormalities,
muscle weakness or paralysis) is essential .
 Once these problems are no longer severe,
the rate of potassium repletion should be
slowed (to 10 meq/h) even though there is
persistent hypokalemia.
 If patient had refractory hypokalemia in
spite of adequate replacement so could
be :
 1/ persistent cause like vomiting or
diuretics
 2/ hypomagnesaemia
 3/ dextrose containing solutions
Hyperkalemia
Definition
 Normal serum potassium 3.5-5.5 mEq/L
 Hyperkalemia is a serum potassium
greater than 5.5 mEq/L
Case 1
A 63 yo male patient with DM, HTN, CHF
has been on digoxin, captopril and
aspirin. Routine work up showed creat.
2.5 mg/dL and K+ 6.5 meq/L.
Q) What are the possible causes of the
hyperkalemia.
Q) How to treat.
electro                           lyte.ppt
symptoms
 severe symptoms of hyperkalemia
usually do not occur until the plasma
potassium concentration is above 7.0
meq/L (unless the rise has been very
rapid).
 severe muscle weakness, or
 marked electrocardiographic changes
ECG changes
 Tall peaked and symmetrical T wave.
(early)
 Progressive slowing of impulse
conduction causing the PR interval to
lengthen and the QRS duration to
increase.
 The P wave may disappear as a result
of atrial standstill or arrest.
electro                           lyte.ppt
ECG changes
 Ultimately the QRS widens further due
to a severe conduction delay and may
become "sine wave," resulting in
ventricular standstill and a flat line
electro                           lyte.ppt
EKG Changes
Peaked T Waves
EKG Changes
Widening of QRS Complex
EKG Changes
Ventricular Tach/Torsades
Treatment of hyperkalemia
 Is the value accurate??
 Are there EKG changes??
 Is there evidence of Hemolysis on lab
specimen??
 Recheck blood
Treatment
 1- Stabilize myocardial membrane
 2- Drive extracellular potassium into the
cells
 3- Removal of Potassium from the body
Case 2
A 35 yo male patient with CRF presented
to the ER with rapid shallow breathing
hypotension and bradycardia found to
have K+ 8.5 meq/L
Q) Which of the following does not affect
K level
Q)which does actually remove K from the
body
1) Ca gluconate 2) NaHCO3
3) Glucose / insulin 4) B-agonists
5)CER (kayexalate) 6) Dialysis
electro                           lyte.ppt
Treatment of hyperkalemia
 Asymptomatic patient with serum K+ of
6.5 meq/L & no ECG changes can be
treated only with a cation exchange
resin (Kayexalate®),
 Patients with a value below 6 meq/L can
often be treated with
 a low potassium diet and
 diuretics.
Treatment of severe
hyperkalemia
Calcium
 Calcium directly antagonizes the
membrane actions of hyperkalemia.
 The protective effect of calcium begins
within minutes, but is relatively short-
lived
Treatment of severe
hyperkalemia
 The usual dose is 10 mL (1 ampul) of a 10 percent
calcium gluconate solution infused slowly over 2 to
3 minutes with constant cardiac monitoring.
 This dose can be repeated after 5 minutes if the
ECG changes persist.(no maximum dose)
 Calcium should not be given in bicarbonate-
containing solutions (leads to calcium carbonate
precipitation).
Treatment of severe
hyperkalemia
Insulin and glucose
 Lowers the plasma K+ concentration by
driving potassium into the cells, by
enhancing the activity of the Na-K-
ATPase pump in skeletal muscle
 10 U plus 50 mL of a 50 percent
glucose solution as a bolus followed by
a glucose infusion to prevent
hypoglycemia
Treatment of severe
hyperkalemia
 Effective therapy usually leads to a 0.5
to 1.5 meq/L fall in the plasma
potassium concentration, an effect that
begins in 15 minutes, peaks at 60
minutes, and lasts for several hours
Treatment of severe
hyperkalemia
Sodium bicarbonate
 Raising the systemic pH with sodium
bicarbonate results in hydrogen ion release
from the cells (as part of the buffering
reaction).
 This change is accompanied by potassium
movement into the cells to maintain
electroneutrality
Treatment of severe
hyperkalemia
 The potassium-lowering action of sodium
bicarbonate is most prominent in
patients with metabolic acidosis.
 It begins within 30 to 60 minutes and
persists for several hours
 is 45 meq (1 ampul of a 7.5 percent
sodium bicarbonate solution) infused
slowly over 5 minutes, repeat in 30
minutes if necessary
Treatment of severe
hyperkalemia
Beta2-adrenergic agonists
 Drive potassium into the cells by
increasing Na-K-ATPase activity.
 Albuterol (10 to 20 mg in 4 mL of saline
by nasal inhalation over 10 minutes
Treatment of severe
hyperkalemia
Cation exchange resin
 sodium polystyrene sulfonate (Kayexalate®).
Takes up potassium and releases sodium.
 Each gram of resin may bind1 meq of K+
and release 1 to 2 meq of sodium.
 The oral dose is usually 20 grams given with
100 mL of a 20 percent sorbitol solution to
prevent constipation, repeat every 4 to 6
hours as necessary.
Treatment of severe
hyperkalemia
 When given as an enema, 50 grams of resin
is mixed with 50 mL of 70 percent sorbitol
plus 100 to 150 mL of tap water.
 This solution should be kept in the colon for
at least 30 to 60 minutes and preferably two
to four hours.
 Each enema can lower the plasma potassium
concentration by as much as 0.5 to 1 meq/L
and can be repeated every two to four hours.
Treatment of refractory
hyperkalemia
Hemodialysis can be used if
 The conservative measures listed above
are ineffective
 Refractory hyperkalemia usually such
patient had very low GFR.
 The patient has marked tissue breakdown
and is releasing large amounts of
potassium from the injured cells
Case 2
A 35 yo male patient with CRF presented
to the ER with rapid shallow breathing
hypotension and bradycardia found to
have K+ 8.5 meq/L
Q) Which of the following does not affect
K level
Q)which does actually remove K from the
body
1) Ca gluconate 2) NaHCO3
3) Glucose / insulin 4) B-agonists
5)CER (kayexalate) 6) Dialysis
electro                           lyte.ppt
Thanks, any question

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electro lyte.ppt

  • 3. Definition  Total body K : 3500 mmole(98% intracellular, 2% extracellular)  Normal serum potassium 3.5-5.5 mEq/L  Hypokalemia is a serum potassium less than 3.5 mEq/L
  • 4.  American diet : 100 mmole  Haemostasis system of K :  1) kidney , intestine  2) Shifting of K between the ECF and ICF
  • 5. Blood pressure Blood pressure Renin Renin Renin Renin Aldo Aldo K K+ + excretion rate and acid excretion rate and acid- - base status ? base status ? H H H Hy y y yp p p po o o ok k k ka a a al l l le e e em m m mi i i ia a a a & & & & P P P Pa a a ar r r ra a a al l l ly y y ys s s si i i is s s s L L L Lo o o ow w w w K K K K+ + + + e e e ex x x xc c c cr r r re e e et t t t i i i io o o on n n n a a a an n n nd d d d n n n no o o or r r r m m m ma a a al l l l a a a ac c c ci i i id d d d- - - -b b b ba a a as s s se e e e    SPP SPP    Barium poisoni Barium poisoning ng    FPP FPP    Hypernatremic HPP Hypernatremic HPP None None Family history Family history Hypernatremia Hypernatremia High K High K+ + excretion and excretion and abnormal acid abnormal acid- -base base Acid Acid- - base state ? base state ? Clue Clue Hyperthyroidism ? Hyperthyroidism ?    TPP TPP YES YES NO NO Metabolic Acidosis Metabolic Acidosis NH NH+ + 4 4 excretion excretion (UAG, UOG) (UAG, UOG) Low Low High High Toluene Toluene Profound diarrhea Profound diarrhea RTA RTA Metabolic Alkalosis Metabolic Alkalosis R Renin enin Normal Normal GS or BS GS or BS Diuretics Diuretics Vomiting Vomiting High High Primary Primary mineralocorticoid excess mineralocorticoid excess Aldo Aldo Aldo Aldo Primary Primary Aldo Aldosteronism steronism Licorice use Licorice use AME AME Ectopic ACTH Ectopic ACTH Liddle syndrome Liddle syndrome Lin SH et al. Am J Emerg Med 2003 ( Lin SH et al. Am J Emerg Med 2003 (
  • 7.  Case 1 A 43 yo male patient with HTN has been on atenolol and HCTZ was found to have a serum K+ 3.2 meq/L.  Case 2 A 55 yo diabetic female was admitted to the ICU with severe vomiting, diarrhea and muscle weakness, initial work up revealed serum K+ 2.1 meq/L.
  • 8. Symptoms Mild to moderate hypokalemia  3 and 3.5 meq/L; this degree of potassium depletion usually produces no symptoms, except for  patients with heart disease ( taking digitalis or undergoing cardiac surgery or  advanced cirrhosis.
  • 9. Treatment of mild to moderate hypokalemia  . In general, the loss of 200 to 400 meq of potassium is required to lower the plasma potassium concentration from 4.0 to 3.0 meq/L  Repletion as oral potassium chloride in divided doses over few days  Treat the underlying cause
  • 10. Treatment of mild to moderate hypokalemia For patients who can’t tolerate oral KCL  I.V KCL where 20 to 40 meq of potassium is added to each liter of fluid. A saline rather than a dextrose solution is preferred for initial therapy, since the administration of dextrose can lead to a transient 0.2 to 1.4 meq/L reduction in the plasma potassium concentration
  • 11. SEVERE HYPOKALEMIA Symptoms  Muscle weakness and paralysis  Renal dysfunction  ECG changes and arrhythmias
  • 12. ECG changes  depression of the ST segment,  decrease in the amplitude of the T wave, and  increase in the amplitude of U waves which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4-V6.
  • 14. Treatment of severe hypokalemia  . A patient with a plasma potassium concentration of 2 meq/L, for example, may have a 400 to 800 meq potassium deficit  The maximum rate of intravenous potassium administration is 10(peripheral line) to 20(central line) meq/h, although higher rates have been given to selected patients with paralysis or life-threatening arrhythmias
  • 15. Treatment of severe hypokalemia  In this setting, solutions containing as much as 200 meq of potassium per liter (20 meq in 100 mL of isotonic saline) have been used. These solutions should be infused into a large vein ( femoral vein, subclavian vein, or internal jugular vein)
  • 16. Treatment of severe hypokalemia  Accidental administration of very large quantities of intravenous potassium can be avoided by limiting the amount of potassium per container (eg, 20 meq in 100 mL of isotonic saline)
  • 17. Treatment of severe hypokalemia  Careful monitoring of the physiologic effects of severe hypokalemia (ECG abnormalities, muscle weakness or paralysis) is essential .  Once these problems are no longer severe, the rate of potassium repletion should be slowed (to 10 meq/h) even though there is persistent hypokalemia.
  • 18.  If patient had refractory hypokalemia in spite of adequate replacement so could be :  1/ persistent cause like vomiting or diuretics  2/ hypomagnesaemia  3/ dextrose containing solutions
  • 20. Definition  Normal serum potassium 3.5-5.5 mEq/L  Hyperkalemia is a serum potassium greater than 5.5 mEq/L
  • 21. Case 1 A 63 yo male patient with DM, HTN, CHF has been on digoxin, captopril and aspirin. Routine work up showed creat. 2.5 mg/dL and K+ 6.5 meq/L. Q) What are the possible causes of the hyperkalemia. Q) How to treat.
  • 23. symptoms  severe symptoms of hyperkalemia usually do not occur until the plasma potassium concentration is above 7.0 meq/L (unless the rise has been very rapid).  severe muscle weakness, or  marked electrocardiographic changes
  • 24. ECG changes  Tall peaked and symmetrical T wave. (early)  Progressive slowing of impulse conduction causing the PR interval to lengthen and the QRS duration to increase.  The P wave may disappear as a result of atrial standstill or arrest.
  • 26. ECG changes  Ultimately the QRS widens further due to a severe conduction delay and may become "sine wave," resulting in ventricular standstill and a flat line
  • 29. EKG Changes Widening of QRS Complex
  • 31. Treatment of hyperkalemia  Is the value accurate??  Are there EKG changes??  Is there evidence of Hemolysis on lab specimen??  Recheck blood
  • 32. Treatment  1- Stabilize myocardial membrane  2- Drive extracellular potassium into the cells  3- Removal of Potassium from the body
  • 33. Case 2 A 35 yo male patient with CRF presented to the ER with rapid shallow breathing hypotension and bradycardia found to have K+ 8.5 meq/L Q) Which of the following does not affect K level Q)which does actually remove K from the body 1) Ca gluconate 2) NaHCO3 3) Glucose / insulin 4) B-agonists 5)CER (kayexalate) 6) Dialysis
  • 35. Treatment of hyperkalemia  Asymptomatic patient with serum K+ of 6.5 meq/L & no ECG changes can be treated only with a cation exchange resin (Kayexalate®),  Patients with a value below 6 meq/L can often be treated with  a low potassium diet and  diuretics.
  • 36. Treatment of severe hyperkalemia Calcium  Calcium directly antagonizes the membrane actions of hyperkalemia.  The protective effect of calcium begins within minutes, but is relatively short- lived
  • 37. Treatment of severe hyperkalemia  The usual dose is 10 mL (1 ampul) of a 10 percent calcium gluconate solution infused slowly over 2 to 3 minutes with constant cardiac monitoring.  This dose can be repeated after 5 minutes if the ECG changes persist.(no maximum dose)  Calcium should not be given in bicarbonate- containing solutions (leads to calcium carbonate precipitation).
  • 38. Treatment of severe hyperkalemia Insulin and glucose  Lowers the plasma K+ concentration by driving potassium into the cells, by enhancing the activity of the Na-K- ATPase pump in skeletal muscle  10 U plus 50 mL of a 50 percent glucose solution as a bolus followed by a glucose infusion to prevent hypoglycemia
  • 39. Treatment of severe hyperkalemia  Effective therapy usually leads to a 0.5 to 1.5 meq/L fall in the plasma potassium concentration, an effect that begins in 15 minutes, peaks at 60 minutes, and lasts for several hours
  • 40. Treatment of severe hyperkalemia Sodium bicarbonate  Raising the systemic pH with sodium bicarbonate results in hydrogen ion release from the cells (as part of the buffering reaction).  This change is accompanied by potassium movement into the cells to maintain electroneutrality
  • 41. Treatment of severe hyperkalemia  The potassium-lowering action of sodium bicarbonate is most prominent in patients with metabolic acidosis.  It begins within 30 to 60 minutes and persists for several hours  is 45 meq (1 ampul of a 7.5 percent sodium bicarbonate solution) infused slowly over 5 minutes, repeat in 30 minutes if necessary
  • 42. Treatment of severe hyperkalemia Beta2-adrenergic agonists  Drive potassium into the cells by increasing Na-K-ATPase activity.  Albuterol (10 to 20 mg in 4 mL of saline by nasal inhalation over 10 minutes
  • 43. Treatment of severe hyperkalemia Cation exchange resin  sodium polystyrene sulfonate (Kayexalate®). Takes up potassium and releases sodium.  Each gram of resin may bind1 meq of K+ and release 1 to 2 meq of sodium.  The oral dose is usually 20 grams given with 100 mL of a 20 percent sorbitol solution to prevent constipation, repeat every 4 to 6 hours as necessary.
  • 44. Treatment of severe hyperkalemia  When given as an enema, 50 grams of resin is mixed with 50 mL of 70 percent sorbitol plus 100 to 150 mL of tap water.  This solution should be kept in the colon for at least 30 to 60 minutes and preferably two to four hours.  Each enema can lower the plasma potassium concentration by as much as 0.5 to 1 meq/L and can be repeated every two to four hours.
  • 45. Treatment of refractory hyperkalemia Hemodialysis can be used if  The conservative measures listed above are ineffective  Refractory hyperkalemia usually such patient had very low GFR.  The patient has marked tissue breakdown and is releasing large amounts of potassium from the injured cells
  • 46. Case 2 A 35 yo male patient with CRF presented to the ER with rapid shallow breathing hypotension and bradycardia found to have K+ 8.5 meq/L Q) Which of the following does not affect K level Q)which does actually remove K from the body 1) Ca gluconate 2) NaHCO3 3) Glucose / insulin 4) B-agonists 5)CER (kayexalate) 6) Dialysis