Potassium and Arrhythmias

Introduction

Both high and low levels of potassium can predispose to the development of arrhythmias.

Hyperkalaemia

Definition

Hyperkalaemia is defined as a serum potassium concentration higher than 5.5 mM.

ECG changes

ECG changes include, from earliest to last changes as potassium levels increase:

1. Tented T waves
2. Short QT and long PR interval
3. P wave flattening
4. Wide QRS
5. Sinusoidal waves

Eventually, there is ventricular fibrillation or asystole that culminate in death.

Pathophysiology

An increasing potassium concentration exerts electrophysiological effects via 2 mechanisms:

1. Membrane depolarisation

The electrochemical potential difference is dictated by the intracellular and extracellular ion concentrations. According to the Nernst equation, an increase in potassium produces resting membrane depolarisation. Membrane depolarisation inactivates sodium channels, which are responsible for the initial action potential depolarisation. This produces P wave flattening, PR prolongation and QRS widening.

2. Faster repolarisation rate

Potassium currents (I_Kr) account for repolarisation of the myocyte. These currents increase through an unknown mechanism as potassium levels increase. Thus, repolarisation is amplified, producing peaked T waves and short QT duration.

Management

Hyperkalaemia should be treated urgently as it can lead to fatal arrhythmias. In severe cases (e.g. potassium levels higher than 6.5 mmol/L and/or symptomatic), IV calcium should be given initially for its cardioprotective effect. Insulin-dextrose solution and salbutamol nebulisers can then be given to reduce serum potassium levels.

Hypokalaemia

Definition

Hyperkalaemia is defined as a serum potassium concentration lower than 3.5 mM.

ECG changes

Includes, from earliest to last changes as potassium levels decrease:

1. T wave flattening
2. U wave appearance
3. ST depression
4. T wave inversion
5. PR prolongation
6. P wave peaking

Delayed myocyte repolarisation paves the way for re-entrant arrhythmias and ventricular fibrillation.

Pathophysiology

A decrease in potassium concentration exerts electrophysiological effects via 2 mechanisms:

1. Membrane hyperpolarisation

The electrochemical potential difference is dictated by the intracellular and extracellular ions concentrations. According to the Nernst equation, a decrease in potassium produces resting membrane hyperpolarisation. Membrane hyperpolarisation increases the availability of sodium channels. These are responsible for the initial action potential depolarisation and membrane excitability. An increased sodium current produces P wave peaking.

2. Slower repolarisation rate

Potassium currents (I_Kr) account for repolarisation of the myocyte. These currents decrease through an unknown mechanism as potassium levels decrease. Thus, repolarisation is slowed down, producing a prolonged QT duration and T wave flattening.

Management

Potassium replacement is required to avoid fatal arrhythmias. This can be provided orally or intravenously.