Management of Hyperkalaemia

and Hypokalaemia
Potassium homeostasis
 Obtained through the diet -GI absorption is complete - daily excess intake of
about 1 mEq/kg/d (60-100 mEq) - is excreted through the kidneys (90%)
and the gut (10%).

 K homeostasis is maintained predominantly through the regulation of renal

excretion. The most important site of regulation is the cortical collecting
tubule where aldosterone receptors are present.

 Excretion is increased by the following:

 -Aldosterone
 -High Na delivery to the distal tubule, eg, diuretics
 -High urine flow, eg, osmotic diuresis
 -High serum K level
 -Delivery of negatively charged ions to the distal tubule, eg, bicarbonate

 Excretion is decreased by the following:

 -Absence of aldosterone
 -Low Na delivery to the distal tubule
 -Low urine flow
 -Low serum K level
 -Renal failure
Pathophysiology-Hyperkalaemia
 3 pathogenetic mechanisms can cause hyperkalemia.

 Excessive intake: relatively high K intake in a patient with impaired

mechanisms for the intracellular shift of K or renal K excretion.

 Decreased excretion: renal failure; ingestion of drugs that interfere

with K excretion, eg, K-sparing diuretics, ACE-I, NSAIDS; or
impaired responsiveness of the distal tubule to aldosterone, eg, type
IV renal tubular acidosis observed with DM, sickle cell disease,
chronic partial urinary tract obstruction.

 Shift from intracellular to extracellular space: rhabdomyolysis and

tumor lysis. However, more often, insulin deficiency or acute
acidosis.
Clinical Features of Hyperkalaemia
 Plasma K >6.5mmol/l needs urgent treatment-but 1st ensure it’s not
an artefact (eg. due to hemolysis inside the bottle)

 Neuromuscular manifestations: Weakness, paraesthesia, areflexia,

ascending paralysis

 Cardiac manifestations: Bradycardia, prolonged of AV conduction,

complete heart block, wide complex tachycardia, ventricular
fibrillation, and asystole

 ECG: tall tented T waves, small P waves, depressed ST segments,

widened QRS complexes, sine waves (biphasic waves, pre-cardiac
arrest)

 ECG has limitation in predicting cardiac toxicity. Thus patient should

be treated even in the absence of ECG changes
Management
 Goals:
- To protect the heart from effects of K by antagonizing its
effects on cardiac conduction (Ca)
- To shift K from ECF to ICF (Na bicarbonate, insulin & glucose)
- To reduce total body K (cation exchange resin & dialysis)
- Treatment is urgent if K>6.5 mmol/L or ECG shows change of
hyperkalaemia
Recommendations
Mild to moderate hyperK (5.5-6.5mmol/L) with no ECG changes:

 low K diet
 Cation exchange-resins
 Correction of acidosis in patient with metabolic acisosis
 +/- Glucose & insulin infusion
 stop drugs which may cause hyperkalaemia
 K-sparing diuretics, spironolactone, triamterene, amiloride
 NSAIDS
 ACE-I
 ARB
 Cyclosporine or tacrolimus
 Pentamidine
 Trimethoprim/sulfamethoxazole
 Heparin
 Ketoconazole
 Metyrapone
 Herbs
Severe Hyperkalaemia (>6.5 mmol/L) or
with ECG changes
 Above treatments
 Immediate Calcium administration
 Glucose and insulin infusion
 Sodium bicarbonate infusion
 Beta agonist therapy
 Dialysis
Calcium administration
 10ml of 10% calcium gluconate IV over 2-5
minutes. A 2nd dose can be given after 5 mins if
no change in ECG is seen. Effect of calcium
occurs within minutes and lasts for 1 hour
 Slower infusion rates in patients on digitalis to
avoid hypercalcaemia-induced digitalis toxicity
 Calcium should not be given before after
bicarbonate in the same IV line to avoid
precipitation
Glucose and Insulin infusion
 Rapid acting insulin 10u + 50cc of 50% dextrose
IV infused over 30-60min (in pt with renal failure,
higher dose of glucose needs to be given, e.g.
100-150 ml of dextrose)
 Onset within 30-60 min & lasts for several hours
 The above regime can be repeated 6-8 hourly
 Bolus hypertonic glucose solution may
transiently exacerbate hyperK by its osmotic
effect on cells
 After insulin & dextrose infusion, maintain pt. on
continuous dextrose infusion, e.g.D5%
Sodium bicarbonate infusion
 IV infusion of bicarbonate 100-200 mmol/l
over 30 min produces metabolic alkalosis
which lowers K in ECF
 Onset of action occurs within 30 min &
lasts for 1-2 hours
 It is less effective in patients with renal
failure
Cation-exchange resins (Resonium A)

 Bind potassium in exchange for another

cation in GI tract, thereby removing K from
body
 Can be given orally (sodium polystyrebe
[Resonium A] 15-30 g 3-4 times daily) or
as enemas (Resonium A 30 -60 g in 200
ml 3-4 times daily)
Hemodialysis or peritoneal dialysis
 When consvative measures fail, underlying
cause is not reversible or in persistent
hyperkalaemia

Beta-agonist therapy
 IV salbutamol 0.5 mg in 15 min or 10 mg neb
( with or without glucose & insulin infusion) has
been shown to be effective in reducing K level
(IV is preferred in pt with ESRD)
 If effective, plasma K will fall by 0.5-1.5 mmol/l in
15-30 min & effect will last for several hours
Pathophysiology -Hypokalaemia
 Poor K intake - seen in very elderly individuals unable to cook for
themselves or unable to chew or swallow well or in pt.s receiving TPN,
where K supplementation may be inadequate for a prolonged period of time.

 Increased excretion – increase renal K losses incl. enhanced Na delivery to

the collecting duct, as with diuretics; mineralocorticoid excess, as with
primary or secondary hyperaldosteronism; or increased urine flow, as with
an osmotic diuresis.

 GI losses – diarrhea,vomiting (produces volume depletion and metabolic

alkalosis)

 Shift from extracellular to intracellular space- Beta-adrenergic stimulation

e.g.AMI, beta-agonists, insulin treatment e.g. DKA, exogenous glucose,
alkalosis, hypokalaemic periodic paralysis-intermittent weakness lasting up
to 72 hours
Clinical Features of Hypokalaemia
 If K < 2.5 mmol/L, urgent treatment is required. Note that
hypokalaemia exacerbates digoxin toxicity.
 Malaise, fatigue
 Neuromuscular disturbances: Weakness, hyporeflexia,
paraesthesias, cramps, restless legs syndrome,
rhabdomyolysis, paralysis
 GI : Constipation, ileus
 Polyuria, plydipsia, metabolic alkalosis
 ECG changes: small or inverted T waves, prominent U
wave, depressed ST segments, prolonged PR intervals
 Arrhythmias: 1st & 2nd degree heart block, AF, ventricular
tachycardia, ventricular fibrillation
Important facts
 1g KCL contains 14 mmol (14 mEq) of K
 If serum K level does not appreciably rise after adequate K therapy
(e.g. 72-96 h after oral therapy), concomitant Mg depletion should
be suspected.
 If hypoK & low urinary K excretion (<20 mmol/L), hypoK of
extrarenal origin must be suspected
 In asymptomatic pt. with K 3-4 mmol/L, who are vulnerable to
cardiac arrythmias e.g. CCF, digitalis treatment (e.g. digoxin), h/o MI
or IHD- K supplements should be recommended
 If K < 3 mmol/L, K supplements should be recommended
 KCl – preffered choice except in metabolic acidosis ( potassium
bicarbonate or potassium citrate is preferred) &
hypophosphataemia, e.g. DKA (use potassium phosphate)
 K is an intracellular ion; a low serum K reflects a much grater total K
deficit
 Correction of large deficits may require several days as up to 50%
of administered K is excreted in the urine
Management
 Oral therapy
-method of choice for mild to moderate depletion (plasma
K>2.5 mmol/L)
-Oral KCl 1-2g hrly until return of serum K to at least 3.5
mmol/L
-Slow release K (1 tab = 8 mmol)
-40-200 mmol daily of KCl may be rqd over periods of
days or weeks e.g. 20-40 mmol 2-4 x daily depending on
severity of depletion ( as frequent as 2-4 hrly may be rqd)
-Monitor K levels closely to prevent hyperK
-K-sparing diuretics (e.g. amiloride, triamterene &
spironolactone) may be an alternative for pt.s in whom
hypoK develops secondary to renal losses
 IV therapy
-Method of choice in pt.s with severe hypoK ( <2.5 mmol/L), with
ECG changes, & in pt.s who are not able to take orally & who are
symptomatic, e.g. cardiac arrythmias with rapid ventricular response,
famililal periodic paralysis, & severe myopathy
-In asymptomatic pt.s without ECG changes, K should be given as
follows:
-at a concentration of < 40 mmol/L (< 3g KCl/L) of dextrose free
carrier fluid
-at a rate of <20 mmol/hr (10 mmol/hr recommended)
-Plasma K should be monitored regularly; ECG monitoring
advised
-In emergency e.g. cardiac arrythmias, severe myopathy,
-K can be given at a rate of 40 mmol/hr (i.e KCl 3 g/hr) & in
concentration of 200-400 mmol/L (by mixing 20-40 mmol or 1.5-3.0
g KCl in 100 ml of saline)
-use large central vein: Femoral venous infusion is preferable than
upper body central vein to avoid deleterious effects on
cardiac conduction
Important notes
 Potential risk of IV K : acute hyperkalaemia, which is
most likely in pt.s with renal insufficiency
 To avoid venous pain, irritation & sclerosis,
concentrations of > 60 mmol/L should not be given
through a peripheral vein
 Preferably fluid should be dextrose free as fast infusion
of dextrose would result in endogenous insulin secretion,
thus simulating an insulin/gllucose infusion.
 IV administration of K at a rate of > 10 mmol/hr requires
continuous ECG monitoring
 As soon as ECG normalize, cardiac rhythm returns to
normal or respiratory muscle strength is restored, IV
infusion is gradually tapered & discontinued. Oral KCl is
then initiated.
Complications:
Complications of hyperkalemia range from mild ECG changes to cardiac
arrest. Weakness is common as well.

 Complications of therapy include the following:

 Failure to control hyperkalemia
 Hypokalemia due to excessively aggressive therapy
 Hypercalcemia due to excessive calcium administration
 Hypocalcemia from excessive bicarbonate therapy
 Chest discomfort or tachycardia due to beta-agonist therapy
 Hypoglycemia or hyperglycemia complicating glucose and insulin administration
 Metabolic alkalosis and tetany due to excessive sodium bicarbonate
administration
 Volume depletion, metabolic alkalosis, renal insufficiency, hypocalcemia,
hypomagnesemia, and hypophosphatemia due to aggressive loop diuretic use
 Colon perforation due to Kayexalate administration
Complications of Hypokalaemia
 Increased susceptibility to cardiac arrhythmias is observed with
hypoK in CCF, IHD/ AMI, aggressive therapy of hyperglycemia,
such as with DKA,digitalis therapy
 Low K intake has been implicated as a risk factor for the
development of HPT and/or HPT EOD.
 Muscle weakness, depression of the deep-tendon reflexes, and
even flaccid paralysis can complicate hypoK. Rhabdomyolysis can
be provoked, especially with vigorous exercise.
 Abnormalities of renal function often accompany acute or chronic
hypoK
 HypoK decreases gut motility, leading to or exacerbating an ileus.
 HypoK also is a contributory factor in the development of hepatic
encephalopathy in the setting of cirrhosis.
 HypoK has a dual effect on glucose regulation.
 HypoK decreases insulin release.
 It also decreases peripheral insulin sensitivity.
 HypoK has widespread actions in many organ systems, which, over
time, result in cardiovascular disease.
Patient Education:
Inform patients regarding the following:
 Instruct patients on symptoms of hypokalemia or hyperkalemia.
 Palpitations or notable cardiac arrhythmias
 Muscle weakness
 Increasing difficulty with diabetes control
 Polyuria
 Dietary sources of K, including salt substitutes
 Medications that impair renal excretion, including ACE-I, ARBs,
NSAIDS, and K-sparing diuretics
 Clinical situations in which pt.s might be at risk for the
development of hyperK, which incl.volume depletion and acute
renal insufficiency complicating GI fluid losses; increasing doses
of ACE-I or K-sparing diuretics; and addition of a medication that
decreases renal excretion or cellular uptake in patients who
already are taking such drugs.