Understanding Hypokalemia and Potassium Regulation

 
 
 
 
 
 
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Potassium…
 
“Chief Intracellular Cation”
 
ECF : 
3.5 – 5.5 
mEq/L (1-2%)
ICF : 
100-150 
mEq/L   (30x / 98%)
 
Chief regulator of ICF/ECF gradient :
Na
+
/K
+
 ATPase Pump
 
 
Total Body Pool Of Potassium : 
3000-
3500
 mEq
 
ICF/ECF Concentration
 
Maintained by 
Na
+
/K
+
 ATPase Pump
 
Cellular K
+
 uptake is rapid and it limits the rapid increase in serum
potassium concentration
 
Shift from ICF to ECF also occurs when serum K
+
 is less
 
Potassium Excretion
 
In a healthy individual at steady state, the entire daily intake of
potassium is excreted
 
Approx. 
90%
 in the urine and 
10%
 
in the stool
 
Kidney
 plays a dominant role in potassium homeostasis
 
Serum Potassium almost completely ionized, not bound to any plasma
proteins: Hence 
effectively filtered by glomerulus
 
1. 
NKCC Channel
 
Active
 
2 Positive 2 negative
 
ion inside
2. 
ROMK Channel
 
takes out K
+
 to lumen
 
positive charge in
 
lumen
3. 
Paracellular Pathway
 
Absorption of Ca
++
 
Mg
++
 
Role of Collecting Duct
 
The collecting duct is the primary site at which the kidney
regulates urinary K+ excretion.
 
 
The collecting duct has the ability both to secrete K+,
enabling adaptation to K+ excess states, and to actively
reabsorb K+, enabling adaptation to K+ depletion states.
 
 
 
The principal cell, particularly in the cortical collecting
duct, secretes potassium, whereas intercalated cells
throughout the entire collecting duct reabsorb
potassium.
 
1.
EnaC
apical Na+ entry
Amiloride sensitive
generates a negative potential
difference in lumen
drives passive K+ exit through
apical K+ channels
2.
ROMK / KiR 1.1
apical K+ channels
the bulk of constitutive K+
secretion
3.
Flow-sensitive big
potassium (BK) or maxi-K K+
channel
increases in distal flow rate
genetic absence of ROMK
 
Factors influencing principal cell potassium secretion
1.
Luminal flow rate (most Important)
2.
Distal sodium delivery
3.
Aldosterone
4.
Extracellular pH
 
Apical H+-K+-ATPase
Reabsorb K
+
 from Lumen
Secretes H
+
Potassium depletion increases
H+-K+-ATPase expression
Aldosterone increases H+-K+-
ATPase expression
 
 
The presence of two separate potassium transport
processes, secretion by principal cells and
reabsorption by intercalated cells, contributes to rapid
and effective regulation of renal potassium excretion.
 
HYPOKALEMIA-
Definition
 
Serum potassium <3.5 mEq/L
 
occurs in up to 20% of hospitalized patients
 
10-fold increase in in-hospital mortality
Causes of Hypokalemia
 
1.
Psuedohypokalemia
2.
Reduced Intake
3.
Increased translocation into cells
4.
Increased Loss
a.
Renal
b.
GIT
c.
Sweat
d.
Dialysis
e.
Plasmapheresis
 
Pseudohypokalemia
 
artefactual decrease in serum potassium, after phlebotomy
 
in vitro cellular uptake of K+ after venipuncture
 
MCC : 
Acute Leukemia
 
Large numbers of abnormal leukocytes take up potassium when the
blood is stored in a collection vial for prolonged periods at room
temperature
 
Reduced Intake
 
Average Person : 40 – 120 mEq/Day
Recommended : Close to 120 mEq/day
Mostly excreted : 
Urine
If Intake low : Kidney excretes Low K
+
 (conserves)
 
“decrease in intake rarely causes hypokalemia”
Decrease in intake can increase the severity of hypokalemia if there is already
existing other causes of hypokalemia
Ex: Diuretic Therapy
 
Translocation into cells
 
Mechanism: 
Na
+
 K
+
 ATPase 
Action
 
Causes:
1.
Increased availability of insulin
2.
Increased Beta Agonist activity
3.
Alpha Antagonism
4.
Alkalosis
5.
Hypokalemic Periodic Paralysis
 
Increased β
2 
Agonism
 
activation of β
2
-adrenergic receptors stimulates Na
+
K
+
 ATPase , inducing
cellular potassium uptake and decreasing serum K+
(Possibly also by increasing the release of insulin 
- UPTODATE
)
 
1
-adrenergic receptor activation has the opposite effect)
 
 
UNEXPECTED HYPOKALEMIA
Β
2
 agonist as 
bronchodilators 
in treatment of asthma
Dobutamine 
in treatment of heart failure
 
 
Tocolytics : 
Ritodrine
Pseudoephedrine and 
ephedrine
 in cough syrup or dieting
agents
Theophylline
 intoxication/ 
Caffeine
 : xanthine- dependent
activation of
 
c-AMP dependent signaling (downstream to 
Β
2
 
receptor
 
Β
2
 agonist must be used with caution in
1.
Hypertensives on diuretic therapy
2.
Preterm labor on treatment with Ritodrine as tocolytic
 
 
Stress induced alterations in the activity of the endogenous
sympathetic nervous system can cause hypokalemia
sometimes :
 
1.
Alcohol withdrawal
2.
Hyperthyroidism
3.
Acute myocardial infarction
4.
Severe head injury
 
Hypokalemic Periodic Paralysis
 
FAMILIAL HYPOKALEMIC
PERIODIC PARALYSIS
Genetic
Profound Hypokalemia
M>F
Never occurs after 25 yrs of age
 
THYROTOXIC PERIODIC
PARALYSIS
 
a/w hyperthyroidsm
Profound hyp
o
kalemia
F>M
 
FAMILIAL HYPOKALEMIC PERIODIC PARALYSIS
 
Missense mutations :
1.
α1 subunit of L-type calcium channels (type 1)
2.
skeletal Na+ channel (type 2)
Acute Attacks in which sudden movement of potassium occurs into
cells
Profound Hypokalemia (1.5 – 2.5)
Precipitated often by rest following exercise stress and carbohydrate
rich meals
Serum potassium normal in between the attacks
Low urinary potassium excretion
 
THYROTOXIC PERIODIC PARALYSIS
 
periodic attacks of hypokalemic paralysis
Asian or Hispanic origin
genetic variation in a thyroid hormone responsive K+ channel : Kir2.6, present
in muscles
weakness of the extremities and limb girdles (frequently between 1 and 6 am)
Signs and symptoms of hyperthyroidism are not invariably present
Mechanisms
1.
activation of the Na+/ K+ ATPase
2.
β-adrenergic activity
High-dose propranolol (3 mg/kg) rapidly reverses the associated hypokalemia,
hypophosphatemia, and paralysis
 
Other causes of transcellular shift
 
Potassium repletion associated “Paradoxical Hypokalemia”
Increased Blood cell production: due to uptake
Vitamin B12/ Folate administration
GM-CSF administration
Hypothermia
Barium intoxication
Cesium intoxication
Chloroquine intoxication
Antipsychotic drugs ( Risperidone, Quetiapine)
 
GI LOSS
 
Upper GI Loss
UGI secretion : 5-10 mEq/L
1.
Vomiting
 
Alone cannot cause
hypokalemia as such
Since K
+
 Conc is very low
 
Lower GI Loss
LGI Secretion : 20 – 50 mEq/L
1.
Diarrhea
2.
Laxatives
3.
Tube drainage
4.
Villous adenoma
5.
VIPoma
6.
Persistent Infective Diarrhea
 
Upper GI Loss
 
Lower GI Loss
 
Mechanism
1.
Bicarbonate Loss
2.
Hyperchloremic Metabolic Acidosis
 
Other Causes of LGI Loss:
1.
Bowel Cleaning for colonoscopy : PEG, Sodium Phosphate
2.
Ogilvies Syndrome
3.
Geophagia
1.Increase Na/Water
delivery
2. Increase Aldosterone Activity
3. Increase
Electronegativity
in Lumen
1.
3.
2. Increase
elecro
Negativity in
lumen
 
Diuretics
 
“any diuretics acting proximal to potassium secreting site can cause
hypokalemia”
1.
CAi
2.
Loop diuretics
3.
Thiazides
 
Mechanism
1.
Increased Na delivery to distal tubule
2.
Volume depletion – RAS stimulation
 
Thiazide Produces more Hypokalemia than Loop diuretics
Reason: Calcium Excretion
Loop diuretics -> calcium excretion-> more calcium in lumen -> electronegativity
in lumen is reduced -> Low K
+
 Excretion
Thiazides -> less calcium excretion -> less calcium in lumen -> more electro
negativity -> More K
+
 Excretion
 
 
Hypokalemia produced by diuretics is dose dependent
Lower dose of thiazides 12.5/25 mg/day of chlorthalidone & hydrochlorthiazide
are now widely used.
Effectively control hypertension
Less Hypokalemia
 
Diuretic induced fluid and electrolyte complications occurs only during
first two weeks of therapy
Steady state attained (if oral intake is adequate)
 
 
“Stable patient with Normal serum potassium at 3 weeks has no risk
of developing late hypokalemia”
Potassium monitoring not required
 Adequate oral intake
No increase in dosing
No other loses (GI: Gastroenteritis)
If any one present: consider temporary cessation of diuretics
 
Increased Mineralo corticoid activity
 
1.
Conns Syndrome
2.
Appareant Mineralo Corticoid Excess
 
Non Reabsorbable Anions in CD
 
1.
Proximal RTA
2.
BetaHydroxyButyrate in DKA
3.
High dose penicillin
4.
Toluene induced metabolic
acidosis (Glue Sniffing):
hippurate
 
Non reabsorbable
Anions Increase
Electronegativity
in Lumen
 
What Happens in DKA ?
 
1.
Glucose -Osmotic Diuretic : More Sodium and water to distal
tubules
 
2.
Dehydration – aldosterone stimulation
 
3.
Ketones - BetaHydroxyButyrate – Non absorbable anion
 
4.
Insulin infusion as treatment
 
Saltwasting Nephropathies
 
1.
Bartter Syndrome
2.
Gittleman Syndrome
3.
Liddle Syndrome
 
HypoMagnesemia
 
Mechanism uncertain
Increase number of open ROMK channels
Magnesium known to 
inhibit ROMK channels
Also can coexist with hypokalemia in upto 
40% 
cases
Concurrent Potassium loses
1.
Diuretic therapy
2.
Tubular toxins : iphosphamide, gentamycin
 
 
AMPHOTERICIN B
: increase permeability of cell membrane collecting
duct
 
LOW CALORIE DIETS: Atkins diet
 
 
Polyuria
 
Clinical Features
 
Muscular
1.
Weakness : hyperpolarization of skeletal muscle
2.
Rhabdomyolysis
Smooth Muscle
1.
Constipation
2.
Bladder Dysfunction
Endocrine
1.
Carbohydrate Intolerance
2.
Diabetes mellitus (Reduced insulin)
 
 
Cardiovascular changes
 
ventricular and atrial arrhythmias
 
predisposes to digoxin toxicity
 
ECG Abnormalities
 
ECG Changes in Hypokalemia
 
D
I
A
G
N
O
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A
P
P
R
O
A
C
H
 
T
O
H
Y
P
O
K
A
L
E
M
I
A
 
 
Goals Of Treatment
 
1.
prevent life threatening complications
 
2.
to replace the associated K
+
 deficit
 
3.
to correct the underlying cause
 
Potassium Preparations
 
Potassium can be administered as
1.
potassium chloride
2.
potassium phosphate 
: hypokalemia and hypophosphatemia
proximal (type 2) RTA
3.
potassium bicarbonate 
: hypokalemia and metabolic acidosis (eg:
renal tubular acidosis / diarrhea)
 
Oral replacement with KCl is the mainstay of therapy in hypokalemia.
 
 
Notably, hypomagnesemic patients are refractory to K
+
 replacement
alone
 
 
 
Concomitant Mg
2+ 
deficiency should 
always 
be corrected with oral or
intravenous repletion.
 
IV KCL therapy
 
1 Amp KCL = 10 ml = 20 mEq
Approximatly 40 mEq of IV KCl raises Serum K
+
 by 0.5 mEq
Indication of IV KCl:
1.
Severe symptomatic Hypokalemia
2.
Unable to take oral medications
Saline is preferred over dextrose
Pain/ Phlebitis (Rates >10mEq/hr)
 
DKA + Hypokalemia
 
Insulin therapy should be delayed till S. potassium is above 3.3
Addition of potassium to NS will make it hypertonic solution. So 40-60
mEq of Potassium/Litre of Half NS is preffered
 
Redistributive hypokalemia
 
Potential complication is rebound hyperkalemia, as the initial process
causing redistribution resolves or is corrected.
Such patients can develop fatal hyperkalemic arrhythmias
 
When excessive activity of the sympathetic nervous system is thought
to play role in redistributive hypokalemia as in:
1.
Thyrotoxic Periodic Paralysis
2.
Theophylline overdose
3.
Acute head injury
High dose propranolol (3 mg/kg) should be considered; this
nonspecific beta blocker will correct hypokalemia without the risk of
rebound hyperkalemia.
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Hypokalemia is a condition characterized by low potassium levels, crucial for intracellular functions. The Na+/K+ ATPase pump maintains the ICF/ECF gradient. Potassium excretion occurs mainly via the kidneys, with minimal variation in proximal tubule reabsorption. The collecting duct plays a vital role in regulating urinary K+ excretion, adapting to excess or depletion states. Key channels and pathways are involved in potassium absorption and secretion processes.


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  1. A PPROA C H TO H YPOK A L E M IA Dr. GOKUL KRISHNAN(JR1) Dr. GOKUL KRISHNAN(JR1)

  2. Potassium Chief Intracellular Cation ECF : 3.5 5.5 mEq/L (1-2%) ICF : 100-150 mEq/L (30x / 98%) Chief regulator of ICF/ECF gradient : Na+/K+ ATPase Pump Total Body Pool Of Potassium : 3000- 3500 mEq

  3. ICF/ECF Concentration Maintained by Na+/K+ ATPase Pump Cellular K+ uptake is rapid and it limits the rapid increase in serum potassium concentration Shift from ICF to ECF also occurs when serum K+ is less

  4. Potassium Excretion In a healthy individual at steady state, the entire daily intake of potassium is excreted Approx. 90% in the urine and 10% in the stool Kidney plays a dominant role in potassium homeostasis Serum Potassium almost completely ionized, not bound to any plasma proteins: Hence effectively filtered by glomerulus

  5. Maximum absorption : PCT (65%) Passive (all ions except Mg++) Other sites: 1. Descending Loop : Secretion 2. TAL (25%) 3. DCT (15%) 4. P cells of Cortical CD (excretion) 5. intercalated cells There is only little variation in proximal tubule potassium reabsorption in response to hypokalemia or hyperkalemia. Major variations occurs at the level of potassium excretion.

  6. 1. NKCC Channel Active 2 Positive 2 negative ion inside 2. ROMK Channel takes out K+ to lumen positive charge in lumen 3. Paracellular Pathway Absorption of Ca++ Mg++

  7. Role of Collecting Duct The collecting duct is the primary site at which the kidney regulates urinary K+ excretion. The collecting duct has the ability both to secrete K+, enabling adaptation to K+ excess states, and to actively reabsorb K+, enabling adaptation to K+ depletion states.

  8. The principal cell, particularly in the cortical collecting duct, secretes potassium, whereas intercalated cells throughout the entire collecting duct reabsorb potassium.

  9. 1. EnaC apical Na+ entry Amiloride sensitive generates a negative potential difference in lumen drives passive K+ exit through apical K+ channels 2. ROMK / KiR 1.1 apical K+ channels the bulk of constitutive K+ secretion 3. Flow-sensitive big potassium (BK) or maxi-K K+ channel increases in distal flow rate genetic absence of ROMK

  10. Factors influencing principal cell potassium secretion 1. Luminal flow rate (most Important) 2. Distal sodium delivery 3. Aldosterone 4. Extracellular pH

  11. Apical H+-K+-ATPase Reabsorb K+ from Lumen Secretes H+ Potassium depletion increases H+-K+-ATPase expression Aldosterone increases H+-K+- ATPase expression

  12. The presence of two separate potassium transport processes, secretion by principal cells and reabsorption by intercalated cells, contributes to rapid and effective regulation of renal potassium excretion.

  13. HYPOKALEMIA-Definition Serum potassium <3.5 mEq/L occurs in up to 20% of hospitalized patients 10-fold increase in in-hospital mortality

  14. Causes of Hypokalemia 1. Psuedohypokalemia 2. Reduced Intake 3. Increased translocation into cells 4. Increased Loss a. Renal b. GIT c. Sweat d. Dialysis e. Plasmapheresis

  15. Pseudohypokalemia artefactual decrease in serum potassium, after phlebotomy in vitro cellular uptake of K+ after venipuncture MCC : Acute Leukemia Large numbers of abnormal leukocytes take up potassium when the blood is stored in a collection vial for prolonged periods at room temperature

  16. Reduced Intake Average Person : 40 120 mEq/Day Recommended : Close to 120 mEq/day Mostly excreted : Urine If Intake low : Kidney excretes Low K+ (conserves) decrease in intake rarely causes hypokalemia Decrease in intake can increase the severity of hypokalemia if there is already existing other causes of hypokalemia Ex: Diuretic Therapy

  17. Translocation into cells Mechanism: Na+ K+ ATPase Action Causes: 1. Increased availability of insulin 2. Increased Beta Agonist activity 3. Alpha Antagonism 4. Alkalosis 5. Hypokalemic Periodic Paralysis

  18. Increased 2 Agonism activation of 2-adrenergic receptors stimulates Na+K+ ATPase , inducing cellular potassium uptake and decreasing serum K+ (Possibly also by increasing the release of insulin - UPTODATE) ( 1-adrenergic receptor activation has the opposite effect) UNEXPECTED HYPOKALEMIA 2 agonist as bronchodilators in treatment of asthma Dobutamine in treatment of heart failure

  19. Tocolytics : Ritodrine Pseudoephedrine and ephedrine in cough syrup or dieting agents Theophylline intoxication/ Caffeine : xanthine- dependent activation of c-AMP dependent signaling (downstream to 2receptor 2 agonist must be used with caution in 1. Hypertensives on diuretic therapy 2. Preterm labor on treatment with Ritodrine as tocolytic

  20. Stress induced alterations in the activity of the endogenous sympathetic nervous system can cause hypokalemia sometimes : 1. 2. 3. 4. Alcohol withdrawal Hyperthyroidism Acute myocardial infarction Severe head injury

  21. Hypokalemic Periodic Paralysis FAMILIAL HYPOKALEMIC PERIODIC PARALYSIS Genetic Profound Hypokalemia M>F Never occurs after 25 yrs of age THYROTOXIC PERIODIC PARALYSIS a/w hyperthyroidsm Profound hypokalemia F>M

  22. FAMILIAL HYPOKALEMIC PERIODIC PARALYSIS Missense mutations : 1. 1 subunit of L-type calcium channels (type 1) 2. skeletal Na+ channel (type 2) Acute Attacks in which sudden movement of potassium occurs into cells Profound Hypokalemia (1.5 2.5) Precipitated often by rest following exercise stress and carbohydrate rich meals Serum potassium normal in between the attacks Low urinary potassium excretion

  23. THYROTOXIC PERIODIC PARALYSIS periodic attacks of hypokalemic paralysis Asian or Hispanic origin genetic variation in a thyroid hormone responsive K+ channel : Kir2.6, present in muscles weakness of the extremities and limb girdles (frequently between 1 and 6 am) Signs and symptoms of hyperthyroidism are not invariably present Mechanisms 1. activation of the Na+/ K+ ATPase 2. -adrenergic activity High-dose propranolol (3 mg/kg) rapidly reverses the associated hypokalemia, hypophosphatemia, and paralysis

  24. Other causes of transcellular shift Potassium repletion associated Paradoxical Hypokalemia Increased Blood cell production: due to uptake Vitamin B12/ Folate administration GM-CSF administration Hypothermia Barium intoxication Cesium intoxication Chloroquine intoxication Antipsychotic drugs ( Risperidone, Quetiapine)

  25. GI LOSS Upper GI Loss Lower GI Loss UGI secretion : 5-10 mEq/L 1. Vomiting LGI Secretion : 20 50 mEq/L 1. Diarrhea 2. Laxatives 3. Tube drainage 4. Villous adenoma 5. VIPoma 6. Persistent Infective Diarrhea Alone cannot cause hypokalemia as such Since K+ Conc is very low

  26. Vomiting : Acid Loss Reduced pH : Metabolic Alkalosis Upper GI Loss Compensation: HCO3- excretion More HCO3-Reaches Collecting duct Hypovolemia More electronegativity in lumen Aldosterone Secretion K+ Excretion K+ Excretion

  27. Lower GI Loss Mechanism 1. Bicarbonate Loss 2. Hyperchloremic Metabolic Acidosis Other Causes of LGI Loss: 1. Bowel Cleaning for colonoscopy : PEG, Sodium Phosphate 2. Ogilvies Syndrome 3. Geophagia

  28. 1. 2. Increase elecro Negativity in lumen 1.Increase Na/Water delivery 3. Increase Electronegativity in Lumen 3. 2. Increase Aldosterone Activity

  29. Diuretics any diuretics acting proximal to potassium secreting site can cause hypokalemia 1. CAi 2. Loop diuretics 3. Thiazides Mechanism 1. Increased Na delivery to distal tubule 2. Volume depletion RAS stimulation

  30. Thiazide Produces more Hypokalemia than Loop diuretics Reason: Calcium Excretion Loop diuretics -> calcium excretion-> more calcium in lumen -> electronegativity in lumen is reduced -> Low K+ Excretion Thiazides -> less calcium excretion -> less calcium in lumen -> more electro negativity -> More K+ Excretion Hypokalemia produced by diuretics is dose dependent Lower dose of thiazides 12.5/25 mg/day of chlorthalidone & hydrochlorthiazide are now widely used. Effectively control hypertension Less Hypokalemia

  31. Diuretic induced fluid and electrolyte complications occurs only during first two weeks of therapy Steady state attained (if oral intake is adequate) Stable patient with Normal serum potassium at 3 weeks has no risk of developing late hypokalemia Potassium monitoring not required Adequate oral intake No increase in dosing No other loses (GI: Gastroenteritis) If any one present: consider temporary cessation of diuretics

  32. Increased Mineralo corticoid activity 1. Conns Syndrome 2. Appareant Mineralo Corticoid Excess

  33. Non Reabsorbable Anions in CD 1. Proximal RTA 2. BetaHydroxyButyrate in DKA 3. High dose penicillin 4. Toluene induced metabolic acidosis (Glue Sniffing): hippurate Non reabsorbable Anions Increase Electronegativity in Lumen

  34. What Happens in DKA ? 1. Glucose -Osmotic Diuretic : More Sodium and water to distal tubules 2. Dehydration aldosterone stimulation 3. Ketones - BetaHydroxyButyrate Non absorbable anion 4. Insulin infusion as treatment

  35. Saltwasting Nephropathies 1. Bartter Syndrome 2. Gittleman Syndrome 3. Liddle Syndrome

  36. HypoMagnesemia Mechanism uncertain Increase number of open ROMK channels Magnesium known to inhibit ROMK channels Also can coexist with hypokalemia in upto 40% cases Concurrent Potassium loses 1. Diuretic therapy 2. Tubular toxins : iphosphamide, gentamycin

  37. AMPHOTERICIN B: increase permeability of cell membrane collecting duct LOW CALORIE DIETS: Atkins diet Polyuria

  38. Clinical Features Muscular 1. Weakness : hyperpolarization of skeletal muscle 2. Rhabdomyolysis Smooth Muscle 1. Constipation 2. Bladder Dysfunction Endocrine 1. Carbohydrate Intolerance 2. Diabetes mellitus (Reduced insulin)

  39. Cardiovascular changes ventricular and atrial arrhythmias predisposes to digoxin toxicity ECG Abnormalities

  40. ECG Changes in Hypokalemia 1. 3.0 3.5 Reduced T wave Amplitude U waves 2. 2.5 3.0 Prolonged QT/QU interval Sagging of ST Segment 3. T and U almost Coalesce 4. <2.5 QRS Widening PR prolongation

  41. DIAGNOSTIC APPROACH TO DIAGNOSTIC APPROACH TO HYPOKALEMIA HYPOKALEMIA

  42. Goals Of Treatment 1. prevent life threatening complications 2. to replace the associated K+ deficit 3. to correct the underlying cause

  43. Potassium Preparations Potassium can be administered as 1. potassium chloride 2. potassium phosphate : hypokalemia and hypophosphatemia proximal (type 2) RTA 3. potassium bicarbonate : hypokalemia and metabolic acidosis (eg: renal tubular acidosis / diarrhea)

  44. Oral replacement with KCl is the mainstay of therapy in hypokalemia. Notably, hypomagnesemic patients are refractory to K+ replacement alone Concomitant Mg2+ deficiency should always be corrected with oral or intravenous repletion.

  45. IV KCL therapy 1 Amp KCL = 10 ml = 20 mEq Approximatly 40 mEq of IV KCl raises Serum K+ by 0.5 mEq Indication of IV KCl: 1. Severe symptomatic Hypokalemia 2. Unable to take oral medications Saline is preferred over dextrose Pain/ Phlebitis (Rates >10mEq/hr)

  46. DKA + Hypokalemia Insulin therapy should be delayed till S. potassium is above 3.3 Addition of potassium to NS will make it hypertonic solution. So 40-60 mEq of Potassium/Litre of Half NS is preffered

  47. Redistributive hypokalemia Potential complication is rebound hyperkalemia, as the initial process causing redistribution resolves or is corrected. Such patients can develop fatal hyperkalemic arrhythmias

  48. When excessive activity of the sympathetic nervous system is thought to play role in redistributive hypokalemia as in: 1. Thyrotoxic Periodic Paralysis 2. Theophylline overdose 3. Acute head injury High dose propranolol (3 mg/kg) should be considered; this nonspecific beta blocker will correct hypokalemia without the risk of rebound hyperkalemia.

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