INFORMATION FOR CANDIDATE:

Your next patient in the emergency department is A 65-

year-old man, Mr. Shaw who presents with generalized
fatigue, muscle weakness and palpitations for 1 week.
He can not recall any acute reason. The only past
history is moderate hypertension for 2 years for which
he was started on an angiotensin-converting enzyme
(ACE) inhibitor 2 months ago but he has missed her
follow-up appointments.

YOUR TASKS ARE TO:

 Take a focused history
 Perform a physcial examination
 Organise appropriate investigations
 Discuss the most likely diagnosis and
management with the patient
HOPC: Mr. Shaw noticed generalized fatigue and muscle weakness and occasional
palpitations over the last week. He can not recall any acute reason and is worried about the
sypmtoms. The only past history is moderate hypertension for 2 years. A recent holter
showed that his average BP was 150/98 and the cardiologist suggested to start an angiotensin-
converting enzyme (ACE) inhibitor 2 months ago. He had no follow-up so far.
PHx. + FHx.: unremarkable
SHx.: married, retired teacher, non drinker, non smoker, NKA, coversyl (perindopril) 4 mg
daily.
EXAMINATION: well looking man in no distress, BP 145/90, P 72 with occasional
extrasystole, afebrile, RR 18, SaO2 98% on RA.
Except for mildly diminished deep tendon reflexes and mildly decreased motor strength the
physical examination is normal.
INVESTIGATIONS:

 ECG: The tracing shows a regular rhythm at 75 bpm. A P wave is present in front of
each QRS complex, indicating that the rhythm is sinus. A flattened P wave (black
arrow), prolonged PR interval (blue bar), borderline widened QRS complexes (green
bar), and -- more pathognomonic -- pointed, narrow, and tented tall T waves (red
arrow) are all features of hyperkalemia.
 The patient's serum potassium when the tracing was recorded was 7.2 mEq/L.

DIAGNOSIS: HPERKALAEMIA:
Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose because
of a paucity of distinctive signs and symptoms. The physician must be quick to consider
hyperkalemia in patients who are at risk for this disease process. Because hyperkalemia can
lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an
immediate ECG to ascertain whether electrocardiographic signs of electrolyte imbalance are
present.
Pathophysiology
Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the
concentration gradient maintained by the sodium- and potassium-activated adenosine
triphosphatase (Na+/K+ –ATPase) pump. The ratio of intracellular to extracellular potassium
is important in determining the cellular membrane potential. Small changes in the
extracellular potassium level can have profound effects on the function of the cardiovascular
and neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body
potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).
Minute-to-minute levels of potassium are controlled by intracellular to extracellular
exchange, mostly by the sodium-potassium pump that is controlled by insulin and beta2
receptors. A balance of GI intake and renal potassium excretion achieves long-term
potassium balance.

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. Ranges are as follows:

 5.5-6.0 mEq/L - Mild condition

 6.1-7.0 mEq/L - Moderate condition
 7.0 mEq/L and greater - Severe condition
Hyperkalemia results from the following:

 Decreased or impaired potassium excretion - As observed with acute or chronic renal

failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell
disease, Addison disease – adrenal insufficiency with hypo-aldosteronism, and
systemic lupus erythematosus (SLE)
 Additions of potassium into extracellular space - As observed with potassium
supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, GIT bleeding,
hyperthermia and haemolysis (eg, venipuncture, blood transfusions, burns, tumor
lysis)
 Transmembrane shifts or ‘redistribution’ (ie, shifting potassium from the intracellular
to extracellular space) - As observed with acidosis (DKA) and medication effects (eg,
acute digitalis toxicity, beta-blockers, succinylcholine)
 Factitious or spurious (pseudohyperkalemia): As observed with improper blood
collection (eg clotted blood, haemolysed or old specimen, blood drawn from iv with
K solution running), laboratory error, leukocytosis, and thrombocytosis

Mortality/Morbidity
 The primary cause of morbidity and death is potassium's effect on cardiac function
(PALPITATIONS, heart block, ventricular arrhythmia or fibrillation, asystole!).
 Neuromuscular weakness.
o Generalized fatigue

o Weakness

o Paresthesias

o Paralysis

MANAGEMENT:

 Ca gluconate 10 mls 10% slowly iv to counteract the potassium effect on

myocardium
 Salbutamol: causes intracellular shift of K: single 5 mg nebulised dose decreases K by
0.2 – 0.4 mmol/L
 NaHCO3: 1 meq/kg over 0.5 hours, the alkalosis causes intracellular shift of K
 Glucose: 100 mls 50% glucose with 20 units short-acting insulin iv or 50 mls 50%
glucose iv. With 5-10 units insulin sc
 Continuous ECG monitoring
 Chronotropes, pacing or adrenaline as required
 If severe renal impairment – haemodialysis!
 Ion exchange resin (RESONIUM) 15-30 g 4-6 hourly, oral or rectal administration