Acute changes in blood pressure as a cause of cardiac arrhythmias

The effect of an acute change in blood pressure (BP) on ventricularectopic activity and the influence of antiarrhythmic agentson this effect were examined in 24 patients. In 11 patientswith premature ventricular complexes (PVCs), the BP was temporarilyreduced by a sodium nitroprusside drip. In all of them the incidenceof PVCs was reduced (or annihilated) by the induced hypotension.In 13 patients without ventricular ectopic activity, a metaraminoldrip was given until either a PVC appeared or the systolic BPreached 200 mmHg, or symptoms appeared. In 12 cases at leastone PVC appeared and in 8 of them the total number of PVCs was13 or more, usually in the form of bigeminy. The repetitionof the test following quinidine administration (serum quinidinelevel 1.7 ±0.5 ng ml^–1) in 6 cases did not changethis pattern, with one exception. It prevented the appearanceof idioventricular accelerated rhythm in one case in whom thisrhythm had been induced by the hypertension provocative testbefore the quinidine administration. All cases, in whom thetest failed to induce more than 3 PVCs, had no cardiac problemat all. Six of the 8 cases in whom the test induced 13 or morePVCs had organic cardiac disease or palpitation. Other arrhythmiasobserved on BP elevation, were supraventricular extra beats,nodal escape rhythms and atrioventricular block. In one casewith cardiomyopathy, the BP elevation was associated with earlysigns of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated withthe generation of PVCs and its reduction with their reductionor disappearance.