The regulation of myocardial
electrolyte concentrations is critical to proper cardiac function.
Myocardial ischemia is associated with deranged ion transport. Left
ventricular assist device (LVAD)
therapy improves myocyte bioenergetics in chronic
heart failure (CHF), which may manifest as
electrolyte alterations; however, rapid
electrolyte shifts may place
critically ill patients at risk for arrhythmias upon initiation of LVAD support. We examine the effect of incremental increases in LVAD support on acute changes in myocardial arteriovenous
electrolytes in CHF. CHF was induced in sheep via coronary microembolization. Four months later, sheep underwent acute LVAD implantation. LVAD support was incrementally increased (0%, 25%, 50%, 75% support). Paired arterial and coronary sinus blood samples were obtained at each increment and analyzed for K+, Ca2+, and Na+ concentrations. Arteriovenous
electrolyte concentrations (mmol/l) were inverted in CHF before LVAD support: K+ (-0.08), Ca2+ (-0.04), and Na+ (0.04). These imbalances were corrected within 20 minutes and with as little as 25% LVAD support: K+ (0.06), Ca2+ (0.012), and Na+ (-0.80). The arteriovenous differences further widened as LVAD support was increased. In conclusion, LVAD support in CHF induces acute alterations in myocardial
electrolytes. Rapid shifts myocardial arteriovenous
electrolyte balances during LVAD support may in part explain the incidence of post-LVAD arrhythmias observed clinically in humans.