Verapamil Worsens Rate of Development and Hemodynamic Effects of Acute Hyperkalemia in Halothane-anesthetized Dogs

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Abstract
The hemodynamic effects of verapamil pretreatment vs. no pretreatment were evaluated in 5 acutely hyperkalemic dogs. Using ECG evidence for severe hyperkalemia, the halothane-anesthetized dogs were rendered acutely hyperkalemic to similar plasma levels of K+ (K+ = 8.2 .+-. 0.8 meq/l verapamil plus hyperkalemia, K+ = 9.4 .+-. 0.2 meq/l hyperkalemic controls). The verapamil-hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 .+-. 0.5 l/min per m2 verapamil plus hyperkalemia vs. CI = 3.0 .+-. 0.2 l/min per m2 hyperkalemic controls) and lower mean arterial pressures (MAP = 60 .+-. 13 mm Hg verapamil plus hyperkalemia vs. MAP 96 .+-. 7 mm Hg hyperkalemic controls). Ca2+ therapy for hyperkalemia that returned CI to control levels in hyperkalemic controls only partially reversed the severe hemodynamic depression and did not improve the AV [atrioventricular] block seen during hyperkalemia in the presence of the Ca entry blocker verapamil. The total meq of KCl infused at the same rate into verapamil-pretrated dogs to result in similar high serum K+ levels was only 1/3 that required in dogs not pretreated with verapamil (1.6 .+-. 0.3 meq/kg KCl in verapamil-hyperkalemia group vs. 5.0 .+-. 0.7 meq/kg KCl in hyperkalemic controls). Evidently verapamil renders hyperkalemia likely after much less i.v. K+ administration. The hemodynamic depression seen during acute hyperkalemia in halothane-anesthetized dogs is much more severe in the presence of verapamil. Ca2+ therapy is only partially effective in reversing the hemodynamic depression caused by hyperkalemia in the presence of Ca2+ entry blocker verapamil; Ca2+ in the dosagse studied was not therapeutic for 2nd-degree A-V block seen in the acutely hyperkalemic dog pretreated with verapamil and anesthetized with halothane.