G6i: Describe the ECG changes seen with hyperkalaemia (30 marks) + Outline the pharmacological principles of drugs used in the management of severe hyperkalaemia (70 marks)

  • Definition ↑K+ = K > 5.5mol/L

Role of K+

  • Major intracellular cation → maintains intracellular tonicity
  • Generation of RMP
  • Na/K/ATPase

Problem of ↑K+

Problem OF ↑K+
  1. RMP is less negative ∴ membrane more excitable
  2. Refractory period initially ↓ but as K > 8mol/L, induces post-repolarisation refraction which prolongs refractory period
  3. Shortened AP duration
  4. ↓conduction velocity
  • V­MAX = rate of rise of AP
  • VMAX ∝ RMP because the membrane potential at onset of depol. determines the no. of Fast Na+ channels activated
  • As RMP becomes less negative = less Na+ channels activated → ↓VMAX
  • ↓VMAX = slows impulse conduction through myocardium

ECG ∆ of ↑K+

K+ (mol/L)

K+ (mol/L)

Reason

5.5 – 6.0

Peaked Tw

Shortened repolarisation

Shortened duration AP

↑myocyte excitability

> 6.5

P waves fluttering

Slowed conduction velocity

> 7.0

Widened QRS

Prolonged PR

Slowed conduction velocity further as ↑RMP

> 8.5

QRS widens further to blend with T-wave → SINE WAVE

Hyperkalaemia MX

Principles of Tx

  1. Stabilise myocardium
  2. More K+ intracellularly
  3. Excrete K+ from body
  4. Tx cause

1) Stabilise myocardium

  • Drug: Ca2+ gluconate 10%
  • Dose: 10mL
  • Onset: 3 mins
  • Duration: 30 – 60 mins
  • MoA: 3 mechanisms
  • Threshold: Ca2+ shifts threshold to be less -ve so difference is maintained
  • VMAX: restoring threshold will normalise VMAX & Na+ channel activation to restore conduction velocity
  • Impulse propagation: Ca2+ dependent AP propagation (SA & AV nodes) restored

2) Move K+ intracellularly

  • Drug: Insulin & D5W
  • Dose: Actrapid 10 units & 50ml of 50% glucose
  • Onset: 10mins
  • Duration: 4-6hrs
  • MoA: Increases Na/K/ATPase activity (3Na out: 2K in) → therefore, drives K intracellularly. Glucose prevents hypoglycaemia
  • Drug: Salbutamol
  • Dose: 5mg neb
  • Onset: immediate
  • Duration: 90mins
  • MoA: Increases activity of Na/K/ATPase of sk m and also activates Na/K/2Cl transporter → therefore drives K intracellularly
  • Drug: NaHCO34%
  • Dose: 50mmol slowly IV over 10 mins
  • Onset: immediate
  • Duration: 30mins
  • MoA: Increases plasma pH → activates K/H antiporter → H extrac/K intrac

3) EXCRETE K+ FROM BODY

  • Drug: Calcium Resonium
  • Dose: 45mg po
  • Onset: 3hrs (max at 12h)
  • Duration: 24hrs
  • MoA: Calcium salt, large & insoluble, binds K+ in colon, prevents reabsorption, promotes excretion
  • Drug: Frusemide
  • Dose: 20-80mg IV
  • Onset: minutes
  • Duration: 2-3hrs
  • MoA:

Inhibits Na/K/2Cl transporter on TAL

Reducing Na & H2O reabsorption

More NaCl reaches collecting duct

Collecting duct tries to reabsorb as much Na+ as possible

-ve charge in lumen left by Cl–

Attracts +ve charge of K+

K+ lost in urine