Acute changes in blood pressure as a cause of cardiac arrhythmias.

The effect of an acute change in blood pressure (BP) on ventricular ectopic activity and the influence of antiarrhythmic agents on this effect were examined in 24 patients. In 11 patients with premature ventricular complexes (PVCs), the BP was temporarily reduced by a sodium nitroprusside drip. In all of them the incidence of PVCs was reduced (or annihilated) by the induced hypotension. In 13 patients without ventricular ectopic activity, a metaraminol drip was given until either a PVC appeared or the systolic BP reached 200 mmHg, or symptoms appeared. In 12 cases at least one PVC appeared and in 8 of them the total number of PVCs was 13 or more, usually in the form of bigeminy. The repetition of the test following quinidine administration (serum quinidine level 1.7 +/- 0.5 ng ml-1) in 6 cases did not change this pattern, with one exception. It prevented the appearance of idioventricular accelerated rhythm in one case in whom this rhythm had been induced by the hypertension provocative test before the quinidine administration. All cases, in whom the test failed to induce more than 3 PVCs, had no cardiac problem at all. Six of the 8 cases in whom the test induced 13 or more PVCs had organic cardiac disease or palpitation. Other arrhythmias observed on BP elevation, were supraventricular extra beats, nodal escape rhythms and atrioventricular block. In one case with cardiomyopathy, the BP elevation was associated with early signs of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated with the generation of PVCs and its reduction with their reduction or disappearance.