Cellular basis for reversal of hyperkalemic electrocardiographic changes by sodium

Abstract

We examined the hypothesis that reversal of hyponatremic hyperkalemic electrocardiographic changes through the infusion of saline solutions was due to the action of sodium ion in increasing the action potential rising velocity which is depressed when the cell is exposed to increasing concentrations of potassium. Using standard microelectrode techniques, the rising velocity of canine ventricular cells was shown to increase by 21%, whereas conduction time between two microelectrodes decreased 17% when the sodium concentration of the perfusate was increased from 120 to 163 mM in 2.7 mM potassium solution. When these cells were exposed to identical increases in sodium concentration in a 7.7-mM potassium solution, rising velocity increased 55% (P less than 0.005), whereas interelectrode conduction time decreased 33% (P less than 0.05). Similar changes were noted in experiments on human ventricular cells. These experimental findings are consistent with the hypothesis stated above.

Effect of Intravenous Small‐Volume Hypertonic Sodium Bicarbonate, Sodium Chloride, and Glucose Solutions in Decreasing Plasma Potassium Concentration in Hyperkalemic Neonatal Calves with Diarrhea

“…This effect together with a delayed potassium-lowering response represents a potential disadvantage of that solution over the use of hypertonic sodium bicarbonate or sodium chloride in calves with acute hyperkalemia and associated cardiac conduction abnormalities as an immediate increase in the sodium-to-potassium ratio is required to reverse the cardiotoxic effects of hyperkalemia. 20,21,77 Also, administration of a hypertonic glucose solution (which has an effective SID of 0 mEq/L) caused a significant decrease in measured plasma SID resulting in a slight acidifying effect, which was also observed in NaCl-treated calves. Although no negative clinical side reactions were observed in glucose-treated calves and all of those calves survived the study, the acidifying and hyponatremic effect of an isolated IV administration of glucose might be even detrimental in calves with a more extreme hyperkalemia than in the 7 calves of the present study (cK 6.8 AE 0.9 mmol/L) because the cardiotoxic effects of hyperkalemia can be exacerbated by the presence of acidemia and hyponatremia.…”

“…This effect together with a delayed potassium‐lowering response represents a potential disadvantage of that solution over the use of hypertonic sodium bicarbonate or sodium chloride in calves with acute hyperkalemia and associated cardiac conduction abnormalities as an immediate increase in the sodium‐to‐potassium ratio is required to reverse the cardiotoxic effects of hyperkalemia 20, 21, 77. Also, administration of a hypertonic glucose solution (which has an effective SID of 0 mEq/L) caused a significant decrease in measured plasma SID resulting in a slight acidifying effect, which was also observed in NaCl‐treated calves.…”

Extracellular sodium and potassium levels modulate cardiac conduction in mice heterozygous null for the Connexin43 gene

“…Hyponatremia has been associated with slowed conduction in the heart [37], presumably by reducing cellular excitability [2]. Reducing cellular excitability could affect the rate of extracellular potential change in the perinexus and thereby weaken ephaptic coupling between myocytes.…”

Hyperkalemia in Dialysis Patients

“…Intravenous hypertonic sodium chloride has been shown to reverse the EKG changes of hyperkalemia in patients with concurrent hyponatremia (80). This effect appears to be mediated by a change in the electrical properties of cardiomyocytes rather than by a reduction in S K (81). Whether hypertonic saline is effective in the treatment of eunatremic patients has not been established.…”