Potassium levels Flashcards

1
Q

What is the definition of hypokalaemia?

A

Serum potassium level <3.5mmol/L

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2
Q

What are the values of moderate hypokalaemia?

A

Moderate hypokalmaeia 2.5 to 3 mmol/L

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3
Q

What are the values of severe hypokalaemia?

A

Severe hypokalaemia <2.5 mmol/L

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4
Q

What is the pathophysiology of hypokalaemia?

A
  1. The ratio of intracellular to extracellular potassium determines the cell membrane potential
  2. Small changes in the extracellular potassium level can have large effects on the cardiovascular and neuromuscular system
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5
Q

What are the causes of hypokalaemia : Increased K+ excretion

A

Losses from the GI tract
Loss of gastric or intestinal secretions from any cause (vomiting, diarrhoea, laxatives, or tube drainage) can cause hypokalaemia.

    • Vomiting: when severe or recurrent can also give rise to renal potassium loss in the setting of metabolic alkalosis.
    • Oral sodium phosphate solution: used for bowel cleansing and is associated with GI losses of potassium.

Increased loss of potassium in urine

  • Diuretics (e.g., acetazolamide, loop diuretics, and thiazide-type diuretics):
  • Urinary potassium excretion increases and may lead to hypokalaemia.
  • Mineralocorticoid excess:
  • urinary potassium wasting is also characteristic of any condition associated with primary hypersecretion of mineralocorticoids (primary aldosteronism)
  • hypersecretion of catecholamines via enhanced release of renin.
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6
Q

How does hypomagnesaemia cause hypokalaemia?

A
  • Hypomagnesaemia can lead to increased urinary potassium loss
  • via an uncertain mechanism, possibly involving an increase in the number of open potassium channels.

determine whether there is hypomagnesaemia because hypokalaemia can often only be corrected once the magnesium deficit has been addressed

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7
Q

Which electroly abnormality coexists with hypokalaemia?

A

serum magnesium <0.75 mmol/L (<1.5 mEq/L) present in up to 40% of patients with hypokalaemia

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8
Q

What are the causes of hypokalaemia due to : Increased K+ entry into the cells

A
  1. Elevation in extracellular pH:
    * Metabolic or respiratory alkalosis - can facilitate potassium entry into cells (hydrogen ions leave the cells and potassium enters into cells to maintain electroneutrality).
  2. Increased beta-adrenergic activity:
  • Catecholamines - promote potassium entry into the cells by increasing Na-K-ATPase activity.
  • Administration of a beta-adrenergic agonist - such as salbutamol or terbutaline (e.g., to treat asthma or to prevent premature labour) or theophylline intoxication can also cause hypokalaemia.
  1. Increased availability of insulin:
    insulin promotes the entry of potassium into skeletal muscle and hepatic cells by increasing the activity of the Na-K-ATPase pump
  2. Hypothermia:
    There have been reports that hypothermia may result in a drive of potassium into cells associated with a plasma potassium concentration decrease to below 3.0 to 3.5 mmol/L (3.0 to 3.5 mEq/L)
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9
Q

What are the miscellaneous causes of hypokalaemia?

A
  1. Chronic alcoholism
    is a common cause of hypokalaemia.
    Hypokalaemia occurs for various reasons, such as poor oral intake, associated vomiting, and secondary hyperaldosteronism.
  2. Maintenance dialysis
    Potassium losses can reach up to 30 mmol/day (30 mEq/day) in patients on chronic peritoneal dialysis. This may become clinically important if potassium intake is reduced or if there are concurrent GI losses
  3. Primary polysipsia/Diabetes insipidus - 2nd to use of antipsychotic medication
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10
Q

What are the clinical features of hypokalaemia?

A
    • Non severe hypokalaemia is often asymptomatic
    • Clinical manifestations of hypokalaemia are typically only seen if serum K+ is <3.0
      * Tetany, muscle weakness, rhabdomyolysis
      * Cardiac arrhythmia
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11
Q

What ECG changes are seen in hypokalaemia?

A
  • ECG changes : wave depression, decrease in amplitude of T wave and increase in amplitude of U waves (seen in late precordial leads V4 - V6)
  • Sinus bradycardia
  • AV block
  • Ventricular tachycardia or fibrillation
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12
Q

What investigations are indicated in hypokalaemia?

A
  1. VBG + bloods
  2. ABG to assess metabolic acidosis/alkalosis
  3. Urine electrolytes to differentiate from renal vs non renal cause
  4. ECG
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13
Q

What is the general cut off for hyperkalaemia?

A

K+ > 5.5 mmol/L

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14
Q

What is the definition of ‘Mild hyperkalaemia’

A

K+ levels of 5.5 - 5.9

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15
Q

What is the definition of ‘Moderate Hyperkalaemia’

A

6.0 - 6.4 mmol/L

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16
Q

What is the definition of ‘Severe Hyperkalaemia’

A

6.5 > mmol/L

17
Q

What is the pathophysiology of hyperkalaemia?

A

Kidney is responsible for maintaining the total body K+ content - any issues with the kidneys lead to impairment in K+ excretion.

18
Q

Which diseases cause hyperkalaemia and why?

A
  1. Acute/Chronic renal failure : impaired excretion of K+
  2. Hypoaldosteronism
19
Q

What is the impact on aldosterone on K+ levels in the blood?

A
  1. Aldosterone acts on late distal tubule and collecting ducts of the nephrons
    - Increased resorption of N+/H20
    - Increases K+ excretion
  2. Increases K+ Ion uptake in the extracellular fluid
20
Q

How do NSAIDS cause hyperkalaemia?

A

NSAIDS : decrease the production of prostaglandins which are involved in the production of aldosterone

21
Q

How may Heparin contribute to hyperkalaemia?

A

Heparin : inhibits renal synthesis of aldosterone thereby decreasing renal K+ secretion

22
Q

Which drugs commonly cause hyperkalaemia? (4)

A
  1. Potassium sparing diuretics : Spirnolactone
  2. RAAS inhibitors : Ace inhibitors, ARBS
  3. NSAIDS : decrease the production of prostaglandins which are involved in the production of aldosterone
  4. Heparin : inhibits renal synthesis of aldosterone thereby decreasing renal K+ secretion
23
Q

Which factors contribute to hyperkalaemia through the mechanism of : Increasing extracellular concentrations of K+

A
  1. Metabolic acidosis
    - Compensatiory mechanism to lower H+ ion levels by moving them into cells via H+/K+ channel
    - Inadvertent increase in K+ in the ECF
  2. Hyperglycaemia/Mannitol
    - Increasing osmolarity in the ECF
    - Increased cellular exit in response to osmotic gradient
  3. Insulin / Beta 2 agonist (Salbutamol)
    - Facilitate for increased cellular uptake of K+ ions
24
Q

How does digoxin overdose cause hyperkalaemia?

A
  • Inhibit N+/K+/ATPase
  • Increase in serum K+ levels
25
Q

What are the risk factors of hyperkalaemia?

A
26
Q

What are the clinical features of hyperkalaemia?

A

Fatigue
Generalised weakness
Chest pain
Palpitations
Signs
Arrhythmias
Reduced power
Reduced reflexes

27
Q

What are the investigation results seen in hyperkalaemia?

A
28
Q

What are the ECG changes in Hyperkalaemia?

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

29
Q

Hyperkalaemia : Management

A

Protect the myocardium
Indic : significant hyperkalaemia (i.e. > 6.5 mmol/L) or ECG changes,
* 10 ml of 10% calcium gluconate over 10 minutes should be given to protect the myocardium

Drive potassium intracellularly
10 units of a short-acting insulin (e.g. ACTRAPID) alongside dextrose (e.g. 50 ml 50% or 100 ml 20%) over 30 minutes.

nebulised salbutamol
activation of beta-receptors, which promotes the intracellular shift of potassium. Salbutamol can be given as back-to-back 5 mg nebulisers at a combined dose of 10-20 mg.

30
Q

What is the management of chronic hyperkalaemia?

A

The only effective ways of eliminating potassium are:

Loop diuretics (e.g. furosemide)
Potassium-binding resins (e.g. Patiromer or sodium zirconium cyclosilicate)
Haemodialysis