Hypo- and Hyperkalaemia Flashcards

1
Q

What are some causes of hyperkalaemia?

A

CARED:
- Cell lysis (haemolysis, burns, surgery, rhabdomyolysis etc); cirrhosis and CCF

  • Adrenal insufficiency/Addison’s disease; Acidosis
  • Renal failure (AKI, chronic)
  • Excessive intake (PO, IVI, blood products)
  • DKA; Dehydration; Drugs
    (BADHAN = Betablockers, ARBs, Digoxin, Heparin, ACEi’s, NSAIDs, Steroid)
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2
Q

How does hyperkalaemia present?

A

Asymptomatic, incidental finding on U+E

MURDER:

  • Muscle weakness + cramps
  • Urine output = decreased
  • Reduced = cardiac output
  • ECG changes
  • Reflexes = decreased
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3
Q

What are the different grades of hyperkalaemia?

A
Mild = 5.5-5.9 
Moderate = 6-6.4 
Severe = >6.5
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4
Q

What ECG changes do you see in hyperkalaemia?

A

K >5.5: repolarisation abnormalities:
- Peaked T waves (usually the earliest sign of hyperkalaemia)

K >6.5: progressive paralysis of the atria

  • Flattening then absent P waves
  • Prolonged PR segment

K >7: conduction abnormalities and bradycardia

  • Prolonged QRS, potentially bizarre morphology
  • Any kind of conduction block e.g. BBBs, fascicular blocks
  • Sinus bradycardia or slow AF
  • Development of a sine wave appearance = pre-terminal rhythm

K >9: causes cardiac arrest

  • V fib
  • Asystole

The concentrations here are just guides, individual variation is common

Changes are usually across all leads

After ECG shows changes will need continuous 3 lead cardiac monitoring + repeat ECG after interventions

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5
Q

What drugs do you give to treat acute hyperkalaemia?

A

Usually used in moderate-high hyperkalaemia; for a mild-moderate, you might want to change diet (if chronic) or stop medicines (if acute)

Calcium gluconate/chloride:

  • 10% by slow IVI
  • Given when plasma-potassium concentration above 6.5 mmol/litre OR in the presence of ECG changes
  • Titrated to ECG improvement
  • To chelate K in the blood - Immediately cardioprotective
  • If the patient is taking digoxin, rapid administration of calcium gluconate may precipitate myocardial digoxin toxicity. The 10 ml of calcium gluconate 10% solution should be mixed with 100ml of glucose 5% and administered slowly over 20 minutes

Insulin + dextrose/glucose:

  • IV injection of 5-10 units with 50ml of 50% glucose over 5-15 mins
  • Repeated as necessary or IVI set up
  • K is taken up alongside sugar into cells in the presence of insulin, will reduce plasma concentration acutely
  • (salbutamol NEB or IVI may accomplish same job but is not preferred)

Sodium bicarbonate:

  • Should be considered for correction of causal or compounding acidosis
  • SHOULD NOT BE ADMINISTERED IN THE SAME LINE AS CALCIUM SALTS - as risk of precipitation

Med review:
- Stop causal/exacerbating agents

Calcium resonium (calcium polystyrene sulfonate):

  • It is given orally at a dose of 15 g three to four times a day (short-term only)
  • To reduce GI absorption
  • Administration of the resin should stop when the serum potassium falls to 5 mmol/litre or below
  • Monitor closely to avoid hypokalaemia
  • Can cause constipation therefore consider co-prescribing laxatives as appropriate
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6
Q

What are the indications for renal replacement therapy in hyperkalaemia?

A

Severe hyperkalaemia that is unresponsive 2-3 rounds of normal measures (??)

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7
Q

What are the causes of hypokalaemia?

A

c. 3% are hypokalaemic on admission to hospital for anything
- This rises to >20% in hospital due to iatrogenic causes e.g. drugs; 1/5 will have severe hypokalaemia

DITCH (the k):

  • Drugs = (LADS) Laxatives, Antibiotics (penicillins and aminoglycosides), Diuretics (loop + thiazides), Steroids
  • Inadequate K+ intake
  • Too much water intake
  • Cushing’s and Conn’s syndromes
  • Heavy fluid losses (NG tube suction, ileostomy, diarrhoea, vomiting, wound drainage etc)
  • Metabolic acidosis
  • Mg depletion
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8
Q

What are the different grades of hypokalaemia?

A

Mild - 3.1-3.5 mmol/L
Moderate - 2.5-3.0 mmol/L
Severe - <2.5 mmol/L

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9
Q

How does hypokalaemia present?

A

Asymptomatic, incidental blood finding
- Often associated with hypomagnesaemia as well

7 L’s:

  • Lethargy
  • Lots of urine
  • Leg cramps
  • Limp muscles
  • Low, shallow breathing
  • Low BP (severe)
  • Lethal cardiac dysrhythmias
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10
Q

What are the ECG features of hypokalaemia?

A

Start occurring when K <2.7mmol/L

  • Increased amplitude + width of P wave
  • Prolongation of PR interval
  • T wave flattening and inversion
  • ST depression
  • Prominent U waves (best seen in V1-3)
  • Apparent long QT due to fusion of T and U waves

In severe:

  • Frequent supraventricular and ventricular ectopics
  • Supraventricular tachyarrhythmias e.g. AF, flutter and atrial tachycardia
  • Potential to develop malignant ventricular rhythms e.g. VT , VF and Torsades de Pointes
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11
Q

How do you manage hypokalaemia?

A

Treat underlying cause e.g. reduction of/withdrawal of diuretics

Dietary change - more fruits/veg, legumes, potatoes, milk, yogurt, nuts

PO supplementation - e.g. Sando-K; regimen depends on extent of deficiency, monitor K daily and adjust accordingly

IV fluids with K+ - if severe deficiency/symptomatic, monitor and titrate accordingly
- Do give K at a rate exceeding 10mmol/h outside of ICU (as can precipitate arrhythmias)

If Mg deficient: you will have to correct this prior to correcting K, else treatment with IV K may appear to improve temporarily but will not last - this is due to Mg being required for co-transport of K

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12
Q

What are some key features of potassium physiology?

A

Mostly intraellular

Vast majority ( >90%) is excreted in the urine

The electrical properties of excitable cells is dependent on the concentration gradient of potassium:
- Therefore, abnormalities may manifest in cell hyperpolarisation or increased duration of the action potential or refractory period

Na/K-ATPase:

  • ATP hydrolysis leads to ADP+Pi+ energy
  • Beta-1 and -2 adrenoreceptors stimulate ATPase, leading to hypokalaemia (low K in serum)

Renal:

  • K absorption in thick ascending limb of LoH
  • Na/K channels in late DCT + collecting duct - K excretion with Na reabsorption; stimulated by aldosterone

Hormonal control:
- Insulin + catecholamines responsible for driving into cells

Acidaemia:
- May result in hyperkalaemia as H+ and K+ are exchanged in tissues

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13
Q

What are some spurious causes of hyperkalaemia?

A

Hemolysis - most common cause of falsely elevated potassium, largely due to pressure gradients created during blood draws performed via syringe or an indwelling cannula

Cold weather/environment, or keeping blood samples in fridge overnight:
- As K leaks out of RBCs into serum)

Thrombocytosis:

  • As K can leach from platelets and megakaryocytes during the clotting process
  • Can use a green top tube instead (?) in these cases, to get a more accurate K
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