Hyperkalemia in Diabetes Mellitus Setting

Figures

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  Figure 1. Distribution of potassium in different body compartments and its inflow and secretion routes.

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  Figure 2. Potassium transport system in the kidneys.

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  Figure 3. Electrocardiographic (ECG) manifestations of hyperkalemia.

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  Figure 4. Diagnostic algorithm in hyperkalemia. Adapted and modified from [31]. GFR—glomerular filtration rate; RTA—renal tubular acidosis; PHA—pseudohypoaldosteronism.

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  Figure 5. Mechanisms of cardiac arrhythmia in hyperkalemia: As K+ levels increase in the ECF (extracellular fluid), the magnitude of K+ gradient across the cell membrane is reduced and so is the absolute value of the membrane potential. Membrane potential becomes less negative moving closer to the threshold potential, making it easier to initiate an action potential. The effect it has on the excitability of myocytes depends on K+ levels. While initial changes seem to increase cardiomyocyte excitability, a further rise in K+ has the opposite effect. This is because the value of the membrane potential at the onset of an action potential determines the number of fast voltage-gated Na+ channels activated during the depolarization. As this value becomes less negative in hyperkalemia, the number of available fast Na+ channels decreases, resulting in a lower influx of Na+ and, subsequently, slower impulse conduction. These changes are associated with an increase in K+ equilibrium potential (EK). ECG changes produced by hyperkalemia follow a typical pattern that generally correlates with K+ serum levels: when fast Na+ channels are activated, an increase in excitability and conduction velocity is…