Potassium Disorders
Dr Hala Ezzat Eid
Professor of Anesthesia and Intensive care
Ain Shams University
Objectives:
By the end of this lecture and reviewing ERC
guidelines you should be able to:
1.
Define normal serum K, hyper/hypokalemia.
2.
Enumerate causes of hyper/hypokalemia.
3.
Recognize hyper/hypokalemia
4.
Discuss management of hyper/hypokalemia and if
any modifications to BLS/AlS .
Normal serum potassium
Extracellular potassium concentration 3.5 and 5.0
mmoll−1 (mmol/L).
N.B.
1mmol = 1mEq for univalent ions e.g. Na+, K+, HCO3
1mmol = 2 mEq for divalent ions e.g. Ca++, Mg++
So always use mmols
Understanding Role of K in membrane potential
Understanding Role of K in membrane potential
 Sodium
is predominantly an extracellular cation
while potassium is predominantly an intracellular
cation
 Cell
membrane is permeable to K but much less to
Na, hence K+ diffuses down its concentration
gradient out of the cell leaving behind negatively
charged proteins. This leads to a potential
difference across the membrane (a negative voltage
on the inside relative to outside). .
Understanding Role of K in membrane potential
 If
K+ continued to leak out of the cell, its chemical
gradient would be lost over time; however, a
Na+/K+-ATPase pump brings the K+ back into the
cell and thereby maintains the K+ chemical
gradient (the pump moves three sodium ions out of
the cell for every two potassium ions it puts in).
Understanding Role of K in membrane potential
 During
action potential Na+ channels open > Na+
enters the cells with reversal of membrane potential
(positive IC)
 Repolarization
takes place mainly by potassium
leaving the cells. Thus K+ has an important role in
repolarization.
Where does potassium in blood come from?

GIT intake

Shift from ICF.
(1) Insulin enhances potassium entry into cells
(2) Beta-adrenergic agonists enhance potassium
entry into cells.
(3) Alkalosis enhances potassium entry into cells
How does the body get rid of potassium?
 1.
Mainly RENAL excretion.
Aldosterone stimulates potassium secretion and
sodium and water retention .
 2.
GIT losses.
 3.
Shift into ICF
N.B.

In acidosis H+ increase in ECF, so H+ move into the
cell and K+ move out of the cell in order to
decrease the acidity.
 Beta-adrenergic agonists enhance potassium entry
into cells (stimulates Na+-K= ATPase)
Understanding diabetic ketoacidosis:
Total body water (TBW) constitutes 60% of total body weight.
For a 70 kg man, TBW = 0.6 x 70 = 42 L
Understanding body fluid compartment
Total body water (TBW) constitutes 60% of total
body weight. For a 70 kg man, TBW = 0.6 x 70 =
42 L
Understanding ACEIs
Hyperkalaemia
 This
is the most common electrolyte disorder
associated with cardiopulmonary arrest.
 Serum
K concentration higher than 5.5mmoll−1
 Severe
hyperkalaemia serum K > 6.5mmoll−1.
Causes of hyperkalemia:
GIT
Diet
IC compartment
Tissue breakdown
(rhabdomyolysis, tumour
lysis, haemolysis),
Stored Packed red blood
cells
Renal
Renal failure
Aldosteron
Addisons
ACE-I
NSAIDs
K sparing diuretics
Metabolic acidosis,
beta-blockers,
Insulin deficiency
N.B. Hemolysis of blood sample can cause Pseudohyperkalemia,
because of the use of torniquet >> recheck in stable patients without
a risk of hyperkalemia.
Hyperkalemia
Excitable Tissues
Effect
Nerve
paraesthesia, depressed deep tendon
reflexes
Sk Muscles
Weakness, paralysis, respiratory failure
Cardiac ms
ECG abnormalities,
arrhythmias, cardiopulmonary arrest or sudden death
Hyperkalemia
 Tall,
peaked T
waves
 Flattened
P waves
 Prolonged
 Widened
PR interval
QRS
Arrhythmias, cardiac
arrest
 N.B.
T
wave represents ventricular repolarization
 High
serum K >> High T wave
Treatment of hyperkalaemia
 There
are three key treatments for hyperkalaemia5:
 1.
cardiac protection;
 2.
shifting potassium into cells;
 3.
removing potassium from the body.
Treatment of hyperkalaemia
CALL FOR HELP
Treatment of hyperkalaemia
 Cardiac
protection (In presence of ECG changes)
Calcium chloride (10%): 10 ml IV over 2 to 5
minutes.
It reduces the effects of potassium at the myocardial
cell membrane and lowers risk of VF.
Treatment of hyperkalaemia
 Shifting
potassium into cells:
1.
Glucose / insulin: 25 g glucose (50 mL of D50 or
100 ml D25) and 10 U regular insulin given IV
over 15 to 30 minutes (onset 15–30 min)
2.
Salbutamol 5mg nebulised. Several doses (10–20
mg) may be required (onset 15–30 min)
3.
Sodium bicarbonate: 50 mmol IV over 5 minutes
if metabolic acidosis present (onset 15–30 min).
Treatment of hyperkalaemia

Promote potassium excretion:
1.
Diuresis: furosemide 40 to 80 mg IV
2.
Potassium exchange resins
3.
Dialysis
Hypokalaemia
 Serum
 Severe
potassium < 3.5mmoll−1.
hypokalaemia is defined as a K+ <
2.5mmoll−1
Causes of hypokalemia
IC compartment
Renal
Aldosteron
GIT
-Poor dietary
intake
-GIT loss
(diarrhoea)
laxatives
-Metabolic alkalosis Renal losses (DI)
-Beta-agonists
Dialysis
-Insulin therapy
Diuretics
-Cushing’s Syndrome
-Hyperaldosteronism
-Steroids
C/P hypokalemia
Excitable Tissues
Effect
Sk Muscles
weakness, cramps
rhabdomyolysis, respiratory failure.
Smooth ms
constipation.
Cardiac ms
ECG abnormalities,
arrhythmias, cardiopulmonary arrest or sudden death
Hypokalemia

U waves
T
wave flattening
 ST-segment
changes
 Arrhythmias, cardiac
arrest
Hypokalemia
N.B.
 The



maximum recommended IV dose of
potassium is 20 mmol per hour in an adult with
continuous ECG monitoring during infusion.
Better via a central line. If using a peripheral line
dilute in 500 ml ringer.
Reassess by measuring serum K.
In severe hypokalemia >> give magnesium 4 mmol
(2 gm ) over 15 minutes i.v.i.
Hypokalemia
N.B>
Rapid infusion (10 mmol over 5 minutes and repeat
once if needed, followed by 10mmol 10min if
needed) is indicated for unstable arrhythmias when
cardiac arrest is imminent.