Cardiac Arrest due to electrolyte disturbance Flashcards

1
Q

Causes of hyperkalaemia?

A
  • Renal dysfunction - AKI, CKD escalation
  • Rhabdomyolysis/tissue breakdown (due to alcoholism, drugs, haemolysis, tumour lysis)
  • Drugs: Use of K sparing diuretics, ACEIs/ARBs etc.
    (β-Blockers, acute digitalis toxicity, succinylcholine, ACE inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory drugs, spironolactone, amiloride)
  • Addison’s (aldosterone -> K+ excretion)
  • Metabolic acidosis
  • Blood transfusions
  • Burns/other RBS destruction disease process.
  • T1DM.
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2
Q

Which patient groups are at risk of cardiac arrest due to hyperkalaemia?

A

Renal failure, severe burn victims, cardiac failure, diabetes mellitus.
Monitor renal function - consider diet/med impacts

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3
Q

Normal range potassium?

A

3.5-5mmol/l

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4
Q

Hyperkalaemia vs severe hyperkalaemia?

A

> 5.5, severe = >6.5

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5
Q

Why do small changes in potassium concentration have big effects?

A

The concentration gradient between K+ in IC space and EC space provides concentration gradient for excitation of tissues

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6
Q

Increase in extracellular potassium - effect on myocytes?

A

Depolarisation.
Initially opens some sodium channels/deactivates some.
Above a certain level: depolarisation inactivates sodium channels and opens potassium channels -> refractory myocytes.

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7
Q

What does refractory mean?

A

Impossible to evoke an AP

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8
Q

At which stage in the cardiac cycle is the myocyte depolarising/refractory?

A

T wave: will not allow another AP to start.

This explains why it is so large on the hyperkalaemic ECG

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9
Q

Why is the P wave flattened/absent in hyperkalaemia?

A

P wave - atrial depolarisation. If myocytes are refractory it cannot depolarise.

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10
Q

What happens to acid/base balance with potassium concentration changes?

A

If serum K is increased -> acidosis.
If it is decreased -> alkalosis.

(K exchanged with H ions to maintain pH)

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11
Q

What is pseudo-hyperkalaemia?

A

Clotting - releases potassium from cells and platelets

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12
Q

Why do beta blockers cause hyperkalaemia?

A

Beta-2 receptor stimulation decreases EC potasisum, if this is blocked then EC potassium will rise.

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13
Q

Why are adrenaline/noradrenaline protective against hyerkalaemia in intense exercise?

A

Due to action on beta-2 receptors: increase uptake of K into cells.

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14
Q

Symptoms of hyperkalaemia?

A

Weakness -> flaccid paralyis
Paresthesia
Confusion
Lethargy

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15
Q

Signs of hyperkalaemia?

A

Weak deep tendon reflexes
ECG abnormalities
Arrthymias
Arrest

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16
Q

ECG changes - what and when?

A

above 6.7 - if ECG is weird this correlates with mortality.
Flat/wide/absent P waves.
PR segment long
Above 7.0 -
Prolonged QRS interval with bizarre QRS morphology
High-grade AV block with slow junctional and ventricular escape rhythms
Any kind of conduction block (bundle branch blocks, fascicular blocks)
Sinus bradycardia or slow AF

17
Q

Sine wave?

A

Indicates cardiac arrest imminent

18
Q

What are 5 key treatments for hyperkalaemia?

A
  1. Protect heart
  2. Shift K into cells
  3. Remove K from body
  4. Monitor K and glucose
  5. Prevent recurrence
19
Q

What to protect heart?

A

IV calcium chloride 10ml 10%

20
Q

Shift into cells?

MOI?

A

Infusion of 10 units insulin with 25g glucose
Salbutamol (10-30mg nebulised)

MOI: increase activity of Na+/K+ATPase pump on cells which drives K+ intracellularly via cAMP

21
Q

Remove K from body

A

? Dialysis/calcium resonium

22
Q

Action of calcium?

A

Antagonises the myocardial effects of potassium and so reduces the threshold potential of cardiac myocytes.

23
Q

4 risks associated with treatment of hyperkalaemia?

A
  1. Hypoglycaemia (usually 1-3hrs after start of treatment)
    Monitor blood glucose
  2. Tissue necrosis if there is extravasation of calcium salts (take care with vascular administration)
  3. Intestinal necrosis or perforation after giving calcium resonium
  4. Rebound hyperkalaemia
24
Q

What are the indications for dialysis for hyperkalaemia?

A

Severe or life threatening hyperkalaemia with or without ECG changes or arrhythmia
Hyperkalaemia resistant to medical treatment
ESRD
Oliguric AKI
Marked tissue breakdown

25
Q

Other than discussed already, what else do you do in CA due to hyperkalaemia?

A

Sodium bicarbonate if severe acidosis/renal failure

26
Q

Risk of giving IV calcium in arrest if not hyperkalaemic?

A

coronary vasospasm and worsening cerebral hypoxic damage

27
Q

What rate can you dialyse and give CPR?

A

200ml/minute

28
Q

Refractory hyperkalaemia?

A

Dialysis!

29
Q

How to perform emergency dialysis?

A

Through central venous catheter: IJV/SCV catheter tip should rest just above RA

30
Q

Most common electrolyte disturbance in general?

A

Hypokalaemia

31
Q

Define hypokalaemia and severe hypokalaemia.

A

Hypo: <3.5
Severe: <2.5

32
Q

Causes of hypokalaemia?

A

GI losses (diarrhoea, laxatives)
Drugs: diuretics, laxatives, steroids.
Renal losses (renal tubular disorders, diabetes insipidus, dialysis)
Endocrine disorders (Cushings, hyperaldosteronism)
Metabolic alkalosis
Magnesium depletion
Poor dietary intake

33
Q

Symptoms/signs of hypokalaemia?

A
ASICWALT
Alkalsosis
Shallow Resp
Irritability
Confusion/drowsiness
Weakness/fatidue
Arrthymias
Lethargy
Thready Pulse
Intestinal motility decreased, nausea, vomiting, ileus
34
Q

Hypokalameia on ECG?

A

Peaked P waves, Prolonged PR, ST depression/prolonged, Depressed T wave (can be inverted) and prominent U wave.

35
Q

Tx of hypokalaemia in imminent arrest/unstable pt?

A

2mmol/min for 10 mins, then 10 mol/5-10 minutes

36
Q

IS CA due to hypokalaemia common?

A

No - mostly in context of eating disorders and diuretic abuse.

37
Q

What electrolyte abnormality do hypokalaemic patients also have?

A

Hypomagnasaemia.

Magnesium is vital in the uptake of K+ and maintainence of cellular potassium values, esp in myocardium
Repletion of magnesium is recommended in severe hypokalaemia as it will facilitate more rapid correction of the disorder