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Flashcards in Hyperkalaemia Deck (20)
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What is the normal range of potassium?

3.5 - 5.5 mmol/L

(Some sources put the upper limit at 5.3 or even 5.0)


What counts as:
- Mild
- Moderate
- Severe

Mild: >5.5
Moderate: >6.0
Severe: >7.0


What are the main clinical manifestations of hyperkalaemia?

Very similar to hypokalaemia:
- weakness in legs, then arms
- cardiac conduction abnormalities: ECG changes and arrhythmias


What are the classic ECG changes associated with hyperkalaemia?

ECG changes follow a discernable stage-like pattern:

First; tall, tented T waves, then

QRS complex widening; bundle branch blocks; AV blocks, then

P wave flattening (and subsequent disappearance), then

Sine wave (as QRS complex blends with T wave)


What other conditions can cause tall tented T-waves?

Early stages of MI
Rarely, a normal variant


Causes of hyperkalaemia

Reduced renal excretion (usually due to severe renal impairment)

Low aldosterone (aldosterone usually blocks renal reabsorption of K; when aldosterone is low, less K is resorbed, and more of it instead lost in the urine)

Release of K from cells (either trans-membrane shift, or cell lysis)


Which of the mechanisms of hyperkalaemia is the most common aetiology?

Impaired renal excretion is by far the most common aetiology of clinically relevant hypokalaemia.


What are the main causes of impaired urinary excretion?

Renal failure

Hypoaldosteronism (aldosterone's job is to retain Na, and get rid of K. If there is insufficient aldosterone, more K gets retained).


What are the main aetiologies of internal redistribution.

Cell lysis (tumour lysis syndrome, rhabdomyolysis)

Medications (B-blockers, digoxin toxicity)

Insulin deficiency




What is pseudohyperkalaemia?

When K moves out of cells during blood drawing.

Mechanical trauma can cause hemolysis of the sample


Outline the diagnostic evaluation of hyperkalaemia:

1. Exclude pseudohyperkalaemia

2. Evaluate renal function and medication list

3. Evaluate for hypoaldosteronism: check renin, aldosterone, and cortisol.


How do you treat hyperkalaemia?

1. Treat underlying cause

2. Buy time with rapid-acting (but transient measures), if there are ECG changes or if K is >6.5.

3. Therapies that remove K from the body


Identify some rapidly-acting (but transient) measures to control hyperkalaemia:

IV calcium (antagonises action of K at cell membrane, so stabilises cardiac function)

Insulin (drives K into cells) (given with glucose to prevent hypoglycaemia)

B2-agonist, such as nebulised salbutamol


How quickly does IV calcium take to work, and how long does it last?

Time to onset: <5 minutes
Duration: 10-30 minutes


How quickly does insulin work (when being used to treat hyperkalaemia)?

Time to onset 15 minutes
Duration: 2 hours


How quickly does salbutamol work (when being used to treat hyperkalaemia)?

Time to onset: 15 minutes
Duration: 2 hours


What does a patient's acid-base status have to do with their K levels?

In response to alkalosis, the body shifts K into the cells, in exchange for H+ ions into the blood. This regulates the alkalosis, but results in hypokalaemia.


What therapies remove K from the body?

Kayexalate (polysterene polymer bound to sodium. The Na is off-loaded in the intestine in exchange for K which is excreted in the faeces).

Diuretics (loop / thiazide) (with or without saline hydration).



When should diuresis be used as a treatment for hyperkalaemia?

Patient must have ALL of the following:

Mild to moderate hyperkalaemia

Renal function not severely impaired (otherwise, diuretics would have limited action)

Patient has other indications for diuresis


When is dialysis appropriate treatment for hyperkalaemia?

End stage renal disease
Severe ECG changes