DISORDERS OF

POTASSIUM
SIU
Dr. YABAROW
Potassium
 K + is the second most abundant cation in the body about 3500 mEq
(50 mEq/kg body weight), (3.5mol).
Daily minimum requirement of K+ is approximately 1600 to 2000 mg
(40 to 50 mEq) (40 mg = 1 mEq).
 Only around 65mmol is present in the ECF,
 The great majority (98%) found within cells in muscle (and, to a
lesser extent, liver, red cells, and bone/cartilage).
 Once absorbed, K + is rapidly buffered by removal from the ECF into
the intracellular compartment:
Potassium
 Insulin and B -adrenergic catecholamines stimulate membrane Na
+ /K + -ATPase to pump K + into cells (in a 3:2 ratio).
 This electrochemical gradient (the cell membrane potential) is
critical to nerve conduction, muscle contraction, and normal cell
function.
 Total body K + balance is regulated by renal excretion:
• K + is freely filtered at the glomerulus (approx. 700mmol/day) and is
reabsorbed by the PCT (75%), the loop of Henle (15%), and the
alpha-intercalated cells of the collecting duct.
Potassium
 K + secretion is responsible for most urinary potassium loss
and is tightly controlled by aldosterone in the DCT and the
principal cells of the collecting duct.
 N.B: Obligate urinary K + loss (10 – 15mmol/day) will always
occur, no matter how low the serum K +.
 Aldosterone secretion is increased directly by hyperkalaemia
(and hypovolaemia) and suppressed by hypokalaemia,
controlling K + in the normal range (3.5 – 5.0mmol/L).
Potassium
 Aldosterone causes Na + absorption through the epithelial sodium
channel.
 As luminal electronegativity increases with Na + absorption, Cl –
uptake is enhanced along paracellular pathways, with secretion of
K + and H + back into the lumen.

Potassium
 Other factors are important in urinary K + excretion:
 Flow in the distal tubule activates stretch-sensitive K + channels
causes increased urinary K + loss.
 Increased tubular sodium delivery leads to increased luminal
sodium-activating ENaC directly.
 ADH or vasopressin may stimulate (some) sodium reabsorption, so
increasing K + loss.
 Alkalosis.
Hyperkalaemia
 True hyperkalaemia is either due to increased release from cells or decreased
excretion by the kidney.
• Pseudohyperkalaemia:
 If there is raised K + in patient, recheck result:
 Venipuncture can cause cellular K + leakage and false hyperkalaemia.
 This can lead to 1 – 2mmol/L rise in the apparent K +.
 Fine-bore needles, tourniquets, and fist clenching can all induce mechanical
release of K + from cells, as can cold temperature.
 More common with high WBC (>100), platelet count (>400 x 10x9 ) or
polycythemia.
Common causes of hyperkalemia include
 CKD per se.
 K + -rich diets (bananas, other fruits) with CKD.
 Drug-induced (esp. combinations of the following):
 ACE inhibitors/ARB.
 K + -sparing diuretics (spironolactone, eplerenone, amiloride).
 NSAIDs.
 Heparin and LMW heparins (inhibit normal aldosterone release).
 Ciclosporin.
 High-dose trimethoprim
 B –blockers
Common causes of hyperkalemia include
 Hypoaldosteronism
 Addison’s.
 Increased release from cells:
 Acidosis (lactic).
• Insulin deficiency (DKA).
• Rhabdomyolysis, strenuous exercise, or tumour lysis.
• Massive haemolysis.
• Succinylcholine use.
Clinical features
 Hyperkalemia is a medical emergency due to its effects on the heart.
 Cardiac arrhythmias associated with hyperkalemia include sinus
bradycardia, sinus arrest, ventricular tachycardia, ventricular fibrillation,
and asystole.
 Mild increases in extracellular K+ affect the repolarization phase of the
cardiac action potential, resulting in changes in T-wave morphology;
 Further increase in plasma K+ concentration depresses intracardiac
conduction, with progressive prolongation of the PR and QRS intervals.
 Severe hyperkalemia results in loss of the P wave and a progressive
widening of the QRS complex;
 Classically, the electrocardiographic manifestations in hyperkalemia
progress from tall peaked T waves (5.5–6.5 mM), to a loss of P
waves (6.5–7.5 mM) to a widened QRS complex (7.0–8.0 mM).
 Hyperkalemia from a variety of causes can also present with
ascending paralysis.
Diagnostic approach
 The first priority in the management of hyperkalemia is to assess
the need for emergency treatment, followed by a comprehensive
workup to determine the cause.
 History and physical examination should focus on:
 medications,
diet and dietary supplements,
risk factors for kidney failure, reduction in urine output,
blood pressure, and volume status.
Diagnostic approach
 Initial laboratory tests should include:
 electrolytes, BUN, creatinine, serum osmolality, Mg2+ and Ca2+, a
complete blood count, and
urinary pH, osmolality, creatinine, and electrolytes.
 A urine Na+ concentration of <20 mM indicates that distal Na+
delivery is a limiting factor in K+ excretion;
volume repletion with 0.9% saline or treatment with furosemide
may be effective in reducing plasma K+ concentration.
TREATMENT OF HYPERKALEMIA
•The treatment of hyperkalemia is divided into three
stages:
1. Immediate antagonism of the cardiac effects of
hyperkalemia (cardioprotection)
2. Rapid reduction in plasma K+ concentration by
redistribution into cells.
3. Removal of potassium.
1. Immediate antagonism of the cardiac effects of hyperkalemia

Intravenous calcium serves to protect the heart, whereas other

measures are taken to correct hyperkalemia.
• Calcium raises the action potential threshold and reduces
excitability, without changing the resting membrane potential.
• The recommended dose is 10 mL of 10% calcium gluconate (3–4 mL
of calcium chloride), infused intravenously over 2–3 min with
cardiac monitoring.
• The effect of the infusion starts in 1–3 min and lasts 30–60 min
1. Immediate antagonism of the cardiac effects of
hyperkalemia

 The dose should be repeated if there is no change in ECG

findings or if they recur after initial improvement.
 Safer method is, 10 mL of 10% calcium gluconate can be
added to 100 mL of 5% dextrose in water (D5%) and
infused over 20–30 min to avoid acute hypercalcemia.
2.Rapid reduction in plasma K+ concentration by
redistribution into cells.
 Insulin lowers plasma K+ concentration by shifting K+ into cells.
 The recommended dose is 10 units of intravenous regular insulin
followed immediately by 50 mL of 50% dextrose.
 The effect begins in 10–20 min, peaks at 30–60 min, and lasts for 4–
6 h.
 Hypoglycemia is common with insulin plus glucose; hence, this
should be followed by an infusion of 10% dextrose at 50–75 mL/h.
2.Rapid reduction in plasma K+ concentration by
redistribution into cells.
 β2-agonists, most commonly albuterol, are effective but underused
agents for the acute management of hyperkalemia.
 The recommended dose for inhaled albuterol is 10–20 mg of
nebulized albuterol in 4mL of normal saline, inhaled over 10 min;
 the effect starts at about 30 min, reaches its peak at about 90 min,
and lasts for 2–6 h.
 Hyperglycemia is a side effect, along with tachycardia.
3. Removal of potassium.
This is typically accomplished using cation exchange resins,
diuretics, and/or dialysis.
 The cation exchange resin sodium polystyrene sulfonate (SPS)
exchanges Na+ for K+ in the gastrointestinal tract and increases the
fecal excretion of K+;
• The recommended dose of SPS is 15–30 g of powder, almost always
given in a premade suspension with 33% sorbitol.
3. Removal of potassium.
 The effect of SPS on plasma K+ concentration is slow; the full effect may take
up to 24 h and usually requires repeated doses every 4–6h.
 Therapy with intravenous saline may be beneficial in hypovolemic
patients with oliguria and decreased distal delivery of Na+, with the
associated reductions in renal K+ excretion.
 Loop and thiazide diuretics can be used to reduce plasma K+ concentration in
volume-replete or hypervolemic patients with sufficient renal function.
 Hemodialysis is the most effective and reliable method to reduce
plasma K+ concentration;
Hypokalaemia
 Hypokalemia, defined as a plasma K+ concentration of <3.5 mM.
 One of the most common electrolyte abnormalities seen, esp. in
patients on diuretics.
 Although K + of 3 – 3.5mmol/L is generally well tolerated,
hypokalaemia of <2.5mmol/L can be life-threatening.
 Hypokalemia is associated with a 10-fold increase in in-hospital
mortality, due to adverse effects on cardiac rhythm, blood pressure,
and cardiovascular morbidity.
CAUSES OF HYPOKALEMIA
• The causes of hypokalemia are broadly
classified into:
1. Decreased intake
2. Redistribution into cells
3. Increased losses
Decreased intake
•A. Starvation
•B. Clay ingestion
Redistribution into cells
•A. Acid-base
•1. Metabolic alkalosis
•B. Hormonal
•1. Insulin
•2. Increased β2-adrenergic sympathetic activity: post– myocardial infarction,
head injury e.t.c.
•3. β2-Adrenergic agonists – bronchodilators, tocolytics.
•C. Anabolic state
•1. Vitamin B12 or folic acid administration (red blood cell production).
Increased loss
•A. Nonrenal
•1. Gastrointestinal loss (diarrhea)- this is significant cause of
hypokalemia in Somalia, especially children.
•2. Integumentary loss (sweat)
Increased loss
•B. Renal
•1. Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt-
wasting nephropathies.
•2. Increased secretion of potassium:
•a. Mineralocorticoid excess: primary hyperaldosteronism (aldosterone-producing
adenomas, primary or unilateral adrenal hyperplasia.
•b. Renin-secreting tumours (high BP in the young).
•c. Cushing’s disease.
•D. Hypomagnesaemia.
Clinical features of hypokalemia
o Hypokalemia has prominent effects on cardiac, skeletal,
and intestinal muscle cells.
o Take a full drug history, particularly for diuretics.
o Exclude diarrhoea, especially in children.
o The physical examination should pay particular attention
to blood pressure, volume status, and signs suggestive of
specific hypokalemic disorders, e.g., Cushing’s syndrome.
Clinical features of hypokalemia
o Common findings/symptoms include:
 Fatigue,
 constipation,
 Proximal muscle weakness, and decreased tone (progressing to
ascending paralysis as K + level drops):
 Hypokalemia results in hyperpolarization of skeletal muscle, thus
impairing the capacity to depolarize and contract; weakness and
even paralysis may ensue.
Clinical features of hypokalemia
 Cardiac arrhythmias, especially if underlying heart disease.
 Chronically, there is high BP, glucose intolerance, and
decreased urinary concentrating ability.
 Electrocardiographic changes in hypokalemia include
broad flat T waves, ST depression, and QT prolongation;
EFFECT OF HYPOKALEMIA ON THE KIDNEY:
 The functional effects of hypokalemia on the kidney can include:
 Na+-Cl– and HCO3 – retention,
polyuria,
 phosphaturia, hypocitraturia, and
an activation of renal ammoniagenesis.
• Bicarbonate retention and other acid-base effects of hypokalemia
can contribute to the generation of metabolic alkalosis.
Investigations
 Initial laboratory evaluation should include:
 Serum electrolytes, BUN, creatinine, serum osmolality, Mg2+, Ca2+,
a complete blood count, and
 Urinary pH, osmolality, creatinine, and electrolytes.
 Renal K+ excretion can be assessed with a 24-h urine collection;
 A 24-h K+ excretion of <15 mmol is indicative of an extrarenal cause
of hypokalemia (e.g. diarrhea).
 Do spot u-K + and u-Cr. Calculate the urinary K/Cr ratio (KCR).
Potassium to creatinine ratio

LAB DIAGNOSIS

KCR (mmol/mmol) <1 Extrarenal

KCR >1, low BP or normal BP Renal (tubular)

KCR >1, High BP Renal (excess mineral corticoids)

Treatment OF HYPOKALEMIA
 The goals of therapy in hypokalemia are:
1. to prevent life threatening and/or serious chronic consequences,
2. to replace the associated K+ deficit, and
3. to correct the underlying cause and/or
4. mitigate future hypokalemia.
 The urgency of therapy depends on the severity of hypokalemia,
associated clinical factors (e.g., cardiac disease, digoxin therapy),
and the rate of decline in serum K+.
MILD HYPOKALEMIA (>2.5mmol/L):
 Oral slow-release potassium chloride 50 – 150mmol/day in divided doses
(treatment limited by GI intolerability).
 Potassium phosphate, oral, may be appropriate in patients with
combined hypokalemia and hypophosphatemia.
 Potassium bicarbonate or potassium citrate should be considered in
patients with concomitant metabolic acidosis.
 The deficit of K+ and the rate of correction should be estimated as
accurately as possible with the equation below.
 Check K + regularly.
 Rule of thumb is to treat until alkalosis resolves.
Severe or symptomatic hypokalaemia (K
<2.5mmol/L)
 The use of intravenous administration should be limited to patients
unable to use the enteral route or in the setting of severe
complications (e.g., paralysis, arrhythmia).
 Intravenous K+-Cl– should always be administered in saline
solutions, rather than dextrose, because the dextrose-induced
increase in insulin can acutely exacerbate hypokalemia.
 IVI 0.9% saline 1L with 20 – 40mmol KCl at no more than 10 –
20mmol KCl/h through peripheral cannula.
Severe or symptomatic hypokalaemia (K
<2.5mmol/L)
 N.B: Danger of rapid onset hyperkalaemia . Recheck K + every 4
hours!
 In volume-restricted patients or those with profound and ongoing
hypokalaemia, KCl can be given into a central vein as 20 –
40mmol/100mL 0.9% saline at not >40mmol/h using a volumetric
pump.
 Must be in high dependency surroundings such as ICU.
POTASSIUM REPLACEMENT THERAPY
 It is mostly deployed in pediatric patients with profound potassium
loss (most commonly due to vomiting and diarrhea).
 Commonly used formula below shows us the total amount of
potassium that a patient requires in 24 hours.
 It is calculated by adding K+ deficit with daily K+ requirement.
• K+ deficit (in mmol) = (K+ normal lower limit − K+ measured) × kg body weight × 0.4.
• Daily requirement= 1 mmol per kilogram.
• Total daily replacement= deficit + daily requirement.
Case 1
• You received a 10 year old girl in the emergency
department suffering from profuse diarrhea and
vomiting. Her plasma potassium level of 1.9 mmol per
liter, her weight is 24Kgs.
1. Calculate the amount of potassium replacement this
patient needs in the next 24 hours?
2. How many ampoules of KCL will she receive in 24
hours?
• N.B: one ampoule of potassium chloride solution contains
20mmol in 10ml.
• K+ deficit (in mmol) = (K+ normal lower limit − K+ measured) × kg body weight × 0.4.
• Daily requirement= 1 mmol per kilogram.

• K+ deficit= 3.5-1.9= 1.6x24= 38.4x0.4= 15.36mmol

• Daily requirement: 24x1= 24
• Total; 24 hour replacement= 15.36+24= 39.36
mmol. 2 ampoule
CASE 2
• 72 year man collapsed in the market after walking for 6 continuous
hours in the heat. Upon arrival at the emergency you measured his
serum potassium level and found it to be 1.6mmol/l.
1. Given that his weight was 62Kgs, calculate his total potassium
replacement for the first 24 hours?
2. How many ampoules of KCL is he going to receive in 24 hours?
3. What fluids will you mix the KCL with?
4. At what time intervals are you going to give him the KCL?
• Deficit= 3.5-1.6 = 1.9x62= 117.8x0.4=
47.12mmol.
• Daily requirement= 1x62= 62
• Total replacement in 24 hrs = 47.12+62=
109.12mmol.
• 5 1/2 ampoules in 24 hours