The hemodynamic effects of verapamil pretreatmentversusno pretreatment were evaluated in five 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/1 verapamil plus hyperkalemia, K+= 9.4 · 0.2 mEq/1 hyperkalemic controls). The verapamil–hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 · 0.5 1 · min−1· m−2verapamil plus hyperkalemiavs.CI = 3.0 · 0.2 1 · min−1· m−2hyperkalemic controls) and lower mean arterial pressures (MAP = 60 · 13 mmHg verapamil plus hyperkalemiavs.MAP = 96 · 7 mmHg hyperkalemic controls). Calcium 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 block seen during hyperkalemia in the presence of the calcium entry blocker verapamil. Surprisingly, the total mEq of KC±l infused at the same rate into verapamil-pretreated dogs to result in similar high serum potassium levels was only one-third that required in dogs not pretreated with verapamil (1.6 · 0.3 mEq/kg KCl in verapamil–hyperkalemia groupvs.5.0 · 0.7 mEq/kg KCl in hyperkalemic controls). The authors conclude 1) verapamil renders hyperkalemia likely after much less intravenous K+administration; 2) the hemodynamic depression seen during acute hyperkalemia in halothane-anesthetized dogs is much more severe in the presence of verapamil; 3) calcium therapy is only partially effective in reversing the hemodynamic depression caused by hyperkalemia in the presence of the Ca++entry blocker verapamil; 4) Ca++in the dosage studied was not therapeutic for second-degree A-V block seen in the acutely hyperkalemic dog pretreated with verapamil and anesthetized with halothane.