The pathophysiology of potassium and magnesium disturbances. A cardiac perspective

Sodium (Na+) and calcium (Ca++) ions are both involved in the activation of cardiac muscle cells. Na+ ions initially depolarise the cell, and the cell-inward flux of Ca++ ions maintains the plateau phase of the action potential. Ca++ ions trigger the release of more Ca++ ions from the sarcoplasmic reticulum. The free Ca++ ions inside the cell subsequently activate the formation of actomyosin complexes and initiate the contraction. Potassium (K+) and magnesium (Mg++) ions modulate the actions of Na+ and Ca++. Hyperkalaemia lowers the membrane potential, and thereby reduces excitability and conduction velocity. Doubling of the K+ concentration may stop the heart, but slightly increased K+ concentrations may increase the risk of arrhythmia. Hypokalaemia reduces potassium conductance of the muscle cell. Instead of hyperpolarising the cell, as one might expect, the myocardium depolarises in a low-K+ solution. Membrane resistance increases and depolarising currents are insufficiently balanced by K+ conductance changes. In the case of low K+, the cells are unstable and excitability is increased. In addition, hypokalaemia increases the risks of digitalis treatment and enhances the arrhythmogenic effect of digitalis. Although cardiac muscle contains a relatively high concentration of Mg++, the free Mg++ concentration is probably low. Outside the cell, the free Mg++ concentration is about 0.5 to 0.7 mmol/L, and there is probably little or no gradient across the cell membrane. A passive carrier-mediated influx of Mg++ ions balanced by an active countertransport keeps intracellular Mg++ concentrations relatively constant. Membrane permeability is low and Mg++ has little direct effect on the membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)